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Jackson Laboratory old male lepr db mice
Old Male Lepr Db Mice, supplied by Jackson Laboratory, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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old male lepr db mice - by Bioz Stars, 2026-07

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$MyD88 deficiency in Lepr db / db mice enhances IL−10 in adipose tissue and liver and decreased circulating adiponectin and DPP4 activity. Adipose tissue, liver, and blood were collected from Lepr +/+ , Lepr db / db , and Lepr db / db MyD88 −/− mice to examine the effects of MyD88 signaling deletion. ( A ) Foxp3 protein expression in stromal vascular fractions (SVFs) isolated from adipose tissue was assessed by Western blotting. ( B ) Densitometric quantification of Foxp3 expression illustrated in ( A ). ( C , D ) IL−10 protein levels in adipose tissue ( C ) and liver ( D ) were measured by ELISA. ( E ) Plasma dipeptidyl peptidase-4 (DPP4) enzymatic activity was determined using a commercial DPP4 activity assay kit (BioVision, Milpitas, CA, USA, # K779-100). ( F ) Circulating adiponectin levels were quantified by ELISA. Data are presented as mean ± SEM. n = 5 mice per group. * p < 0.05, ** p < 0.01, *** p < 0.001. Foxp3, forkhead box P3.$

Journal: International Journal of Molecular Sciences

Article Title: MyD88 Inhibition Ameliorates Diabetes-Induced Hepatic Inflammation and Gluconeogenesis Through Adipose IL-10 Induction

doi: 10.3390/ijms27062883

Figure Lengend Snippet: MyD88 deficiency in Lepr db / db mice enhances IL−10 in adipose tissue and liver and decreased circulating adiponectin and DPP4 activity. Adipose tissue, liver, and blood were collected from Lepr +/+ , Lepr db / db , and Lepr db / db MyD88 −/− mice to examine the effects of MyD88 signaling deletion. ( A ) Foxp3 protein expression in stromal vascular fractions (SVFs) isolated from adipose tissue was assessed by Western blotting. ( B ) Densitometric quantification of Foxp3 expression illustrated in ( A ). ( C , D ) IL−10 protein levels in adipose tissue ( C ) and liver ( D ) were measured by ELISA. ( E ) Plasma dipeptidyl peptidase-4 (DPP4) enzymatic activity was determined using a commercial DPP4 activity assay kit (BioVision, Milpitas, CA, USA, # K779-100). ( F ) Circulating adiponectin levels were quantified by ELISA. Data are presented as mean ± SEM. n = 5 mice per group. * p < 0.05, ** p < 0.01, *** p < 0.001. Foxp3, forkhead box P3.

Article Snippet: Lepr db/+ mice were obtained from The Jackson Laboratory (Bar Harbor, ME, USA) and bred to generate diabetic Lepr db/db and non-diabetic Lepr +/+ mice littermates.

Techniques: Activity Assay, Expressing, Isolation, Western Blot, Enzyme-linked Immunosorbent Assay, Clinical Proteomics

MyD88 depletion suppresses hepatic inflammatory and gluconeogenic gene expression in Lepr db / db mice. Liver tissues from Lepr +/+ , Lepr db / db , and Lepr db / db MyD88 −/− mice were harvested for quantitative PCR (Q-PCR) analysis. Hepatic mRNA expression levels of inflammatory markers ( ICAM , IL − 1β , TNF − α , IL − 6 , iNOS ), metabolic regulators ( DPP4 , FGF21 ), and gluconeogenic enzymes ( G6pc and Pck1 ) were determined. Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001.

Journal: International Journal of Molecular Sciences

Article Title: MyD88 Inhibition Ameliorates Diabetes-Induced Hepatic Inflammation and Gluconeogenesis Through Adipose IL-10 Induction

doi: 10.3390/ijms27062883

Figure Lengend Snippet: MyD88 depletion suppresses hepatic inflammatory and gluconeogenic gene expression in Lepr db / db mice. Liver tissues from Lepr +/+ , Lepr db / db , and Lepr db / db MyD88 −/− mice were harvested for quantitative PCR (Q-PCR) analysis. Hepatic mRNA expression levels of inflammatory markers ( ICAM , IL − 1β , TNF − α , IL − 6 , iNOS ), metabolic regulators ( DPP4 , FGF21 ), and gluconeogenic enzymes ( G6pc and Pck1 ) were determined. Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Lepr db/+ mice were obtained from The Jackson Laboratory (Bar Harbor, ME, USA) and bred to generate diabetic Lepr db/db and non-diabetic Lepr +/+ mice littermates.

Techniques: Gene Expression, Real-time Polymerase Chain Reaction, Expressing

MyD88 deficiency reduces inflammatory gene expression in Kupffer cells and attenuates liver injury in Lepr db / db mice. Kupffer cells and blood samples were isolated from Lepr +/+ , Lepr db / db , and Lepr db / db MyD88 −/− mice. ( A ) mRNA expression of inflammatory mediators ( IL − 1β , TNF − α , IL − 6 , iNOS , and DPP4 ) in Kupffer cells was quantified by Q-PCR. ( B ) Serum alanine aminotransferase (ALT) levels were measured as an indicator of hepatic injury. Data are presented as mean ± SEM. n = 5 mice per group. * p < 0.05, ** p < 0.01, *** p < 0.001. ALT alanine aminotransferase, AST aspartate transaminase.

Journal: International Journal of Molecular Sciences

Article Title: MyD88 Inhibition Ameliorates Diabetes-Induced Hepatic Inflammation and Gluconeogenesis Through Adipose IL-10 Induction

doi: 10.3390/ijms27062883

Figure Lengend Snippet: MyD88 deficiency reduces inflammatory gene expression in Kupffer cells and attenuates liver injury in Lepr db / db mice. Kupffer cells and blood samples were isolated from Lepr +/+ , Lepr db / db , and Lepr db / db MyD88 −/− mice. ( A ) mRNA expression of inflammatory mediators ( IL − 1β , TNF − α , IL − 6 , iNOS , and DPP4 ) in Kupffer cells was quantified by Q-PCR. ( B ) Serum alanine aminotransferase (ALT) levels were measured as an indicator of hepatic injury. Data are presented as mean ± SEM. n = 5 mice per group. * p < 0.05, ** p < 0.01, *** p < 0.001. ALT alanine aminotransferase, AST aspartate transaminase.

Article Snippet: Lepr db/+ mice were obtained from The Jackson Laboratory (Bar Harbor, ME, USA) and bred to generate diabetic Lepr db/db and non-diabetic Lepr +/+ mice littermates.

Techniques: Gene Expression, Isolation, Expressing

$Altered cytokine expression in adipose SVFs from Lepr db/db MyD88 −/− mice and modulation by IL−10 treatment SVFs were harvested from the adipose tissue of Lepr db/db and Lepr db/db MyD88 −/− mice and purified for mRNA expression of different cytokines by Q-PCR analysis to examine IL-6 , IL − 33 , Foxp3 , CCL2 , IL − 1β , TNF − α , and PDGFα cytokine mRNA expression in adipose SVFs and MyD88 involvement. Furthermore, SVFs (2 × 10 7 cells) purified from the adipose tissue of Lepr db/db and Lepr db/db MyD88 −/− mice were treated with PBS or 10 and 100 ng of IL−10 for 3.5 h followed by Q-PCR analysis of IL − 6 , IL − 33 , Foxp3 , CCL2 , IL − 1β , TNF − α , and PDGFα mRNA expression. n = 5/group. ** p < 0.01, *** p < 0.001. SVF, stromal vascular fraction; forkhead box p3, Foxp3; PDGF, platelet-derived growth factor.$

Journal: International Journal of Molecular Sciences

Article Title: MyD88 Inhibition Ameliorates Diabetes-Induced Hepatic Inflammation and Gluconeogenesis Through Adipose IL-10 Induction

doi: 10.3390/ijms27062883

Figure Lengend Snippet: Altered cytokine expression in adipose SVFs from Lepr db/db MyD88 −/− mice and modulation by IL−10 treatment SVFs were harvested from the adipose tissue of Lepr db/db and Lepr db/db MyD88 −/− mice and purified for mRNA expression of different cytokines by Q-PCR analysis to examine IL-6 , IL − 33 , Foxp3 , CCL2 , IL − 1β , TNF − α , and PDGFα cytokine mRNA expression in adipose SVFs and MyD88 involvement. Furthermore, SVFs (2 × 10 7 cells) purified from the adipose tissue of Lepr db/db and Lepr db/db MyD88 −/− mice were treated with PBS or 10 and 100 ng of IL−10 for 3.5 h followed by Q-PCR analysis of IL − 6 , IL − 33 , Foxp3 , CCL2 , IL − 1β , TNF − α , and PDGFα mRNA expression. n = 5/group. ** p < 0.01, *** p < 0.001. SVF, stromal vascular fraction; forkhead box p3, Foxp3; PDGF, platelet-derived growth factor.

Article Snippet: Lepr db/+ mice were obtained from The Jackson Laboratory (Bar Harbor, ME, USA) and bred to generate diabetic Lepr db/db and non-diabetic Lepr +/+ mice littermates.

Techniques: Expressing, Purification, Derivative Assay

Local IL−10 administration induces Foxp3 expression and suppresses inflammatory signaling pathways in adipose SVFs of Lepr db/db mice. PBS or IL−10 (10, 50, or 100 ng) was injected directly into adipose tissue of Lepr db/db mice. SVFs were isolated 7 days after injection. ( A ) mRNA expression of inflammatory cytokines ( IL − 6 , IL-33 , CCL2 , IL − 1β , TNF − α ) and Foxp3 was quantified by Q-PCR. ( B ) Protein expression of phosphorylated and total JNK and NF-κB was evaluated by Western blotting to assess inflammatory signaling activity. Data are presented as mean ± SEM. n = 5 mice per group. * p < 0.05, ** p < 0.01, *** p < 0.001.

Journal: International Journal of Molecular Sciences

Article Title: MyD88 Inhibition Ameliorates Diabetes-Induced Hepatic Inflammation and Gluconeogenesis Through Adipose IL-10 Induction

doi: 10.3390/ijms27062883

Figure Lengend Snippet: Local IL−10 administration induces Foxp3 expression and suppresses inflammatory signaling pathways in adipose SVFs of Lepr db/db mice. PBS or IL−10 (10, 50, or 100 ng) was injected directly into adipose tissue of Lepr db/db mice. SVFs were isolated 7 days after injection. ( A ) mRNA expression of inflammatory cytokines ( IL − 6 , IL-33 , CCL2 , IL − 1β , TNF − α ) and Foxp3 was quantified by Q-PCR. ( B ) Protein expression of phosphorylated and total JNK and NF-κB was evaluated by Western blotting to assess inflammatory signaling activity. Data are presented as mean ± SEM. n = 5 mice per group. * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Lepr db/+ mice were obtained from The Jackson Laboratory (Bar Harbor, ME, USA) and bred to generate diabetic Lepr db/db and non-diabetic Lepr +/+ mice littermates.

Techniques: Expressing, Protein-Protein interactions, Injection, Isolation, Western Blot, Activity Assay

IL−10 injection increases regulatory T cell accumulation in adipose tissue of Lepr db/db mice. PBS or IL−10 (10, 50, or 100 ng) was injected into adipose tissue of Lepr db/db mice. SVFs were isolated 7 days after injection and analyzed by flow cytometry. ( A ) Representative flow cytometry plots showing CD4 + regulatory T cells (Tregs). ( B ) Quantification of the frequency and absolute number of CD4 + Tregs in adipose tissue. Data are presented as mean ± SEM. N = 5 mice per group. * p < 0.05, ** p < 0.01, *** p < 0.001.

Journal: International Journal of Molecular Sciences

Article Title: MyD88 Inhibition Ameliorates Diabetes-Induced Hepatic Inflammation and Gluconeogenesis Through Adipose IL-10 Induction

doi: 10.3390/ijms27062883

Figure Lengend Snippet: IL−10 injection increases regulatory T cell accumulation in adipose tissue of Lepr db/db mice. PBS or IL−10 (10, 50, or 100 ng) was injected into adipose tissue of Lepr db/db mice. SVFs were isolated 7 days after injection and analyzed by flow cytometry. ( A ) Representative flow cytometry plots showing CD4 + regulatory T cells (Tregs). ( B ) Quantification of the frequency and absolute number of CD4 + Tregs in adipose tissue. Data are presented as mean ± SEM. N = 5 mice per group. * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Lepr db/+ mice were obtained from The Jackson Laboratory (Bar Harbor, ME, USA) and bred to generate diabetic Lepr db/db and non-diabetic Lepr +/+ mice littermates.

Techniques: Injection, Isolation, Flow Cytometry

IL−10 administration decreased blood adiponectin levels and DPP4 activity in Lepr db/db mice. PBS or IL−10 (10, 50, or 100 ng) was injected into adipose tissue of Lepr db/db mice, and tissues were harvested 7 days later. ( A ) IL-10 protein levels in adipose tissue were measured by ELISA. ( B ) Plasma adiponectin levels were determined by ELISA. ( C ) Plasma DPP4 enzymatic activity was assessed using a DPP4 activity assay kit (BioVision, Milpitas, CA, USA, # K779-100). Data are presented as mean ± SEM. n = 5 mice per group. * p < 0.05, ** p < 0.01.

Journal: International Journal of Molecular Sciences

Article Title: MyD88 Inhibition Ameliorates Diabetes-Induced Hepatic Inflammation and Gluconeogenesis Through Adipose IL-10 Induction

doi: 10.3390/ijms27062883

Figure Lengend Snippet: IL−10 administration decreased blood adiponectin levels and DPP4 activity in Lepr db/db mice. PBS or IL−10 (10, 50, or 100 ng) was injected into adipose tissue of Lepr db/db mice, and tissues were harvested 7 days later. ( A ) IL-10 protein levels in adipose tissue were measured by ELISA. ( B ) Plasma adiponectin levels were determined by ELISA. ( C ) Plasma DPP4 enzymatic activity was assessed using a DPP4 activity assay kit (BioVision, Milpitas, CA, USA, # K779-100). Data are presented as mean ± SEM. n = 5 mice per group. * p < 0.05, ** p < 0.01.

Article Snippet: Lepr db/+ mice were obtained from The Jackson Laboratory (Bar Harbor, ME, USA) and bred to generate diabetic Lepr db/db and non-diabetic Lepr +/+ mice littermates.

Techniques: Activity Assay, Injection, Enzyme-linked Immunosorbent Assay, Clinical Proteomics

IL−10 administration suppresses hepatic ICAM , TNF − α , IL − 6 , DPP4 , and iNOS mRNA expression and activates insulin-related signaling pathways in Lepr db/db mice. PBS or IL-10 (10, 50, or 100 ng) was injected into adipose tissue of Lepr db/db mice, and livers were harvested 7 days later. ( A ) Hepatic mRNA expression of ICAM , FGF21 , IL − 1β , TNF − α , DPP4 , and iNOS was determined by Q-PCR. ( B ) Protein expression of phosphorylated and total Akt, STAT3, and ERK was assessed by Western blotting. ( C ) Quantification of the pAkt/Akt and pSTAT3/STAT3 ratio. Data are presented as mean ± SEM. n = 4 mice per group. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Journal: International Journal of Molecular Sciences

Article Title: MyD88 Inhibition Ameliorates Diabetes-Induced Hepatic Inflammation and Gluconeogenesis Through Adipose IL-10 Induction

doi: 10.3390/ijms27062883

Figure Lengend Snippet: IL−10 administration suppresses hepatic ICAM , TNF − α , IL − 6 , DPP4 , and iNOS mRNA expression and activates insulin-related signaling pathways in Lepr db/db mice. PBS or IL-10 (10, 50, or 100 ng) was injected into adipose tissue of Lepr db/db mice, and livers were harvested 7 days later. ( A ) Hepatic mRNA expression of ICAM , FGF21 , IL − 1β , TNF − α , DPP4 , and iNOS was determined by Q-PCR. ( B ) Protein expression of phosphorylated and total Akt, STAT3, and ERK was assessed by Western blotting. ( C ) Quantification of the pAkt/Akt and pSTAT3/STAT3 ratio. Data are presented as mean ± SEM. n = 4 mice per group. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: Lepr db/+ mice were obtained from The Jackson Laboratory (Bar Harbor, ME, USA) and bred to generate diabetic Lepr db/db and non-diabetic Lepr +/+ mice littermates.

Techniques: Expressing, Protein-Protein interactions, Injection, Western Blot

IL−10 injection reduces inflammatory gene expression in Kupffer cells and improves liver injury markers in Lepr db/db mice. PBS or IL−10 (10, 50, or 100 ng) was injected into adipose tissue of Lepr db/db mice. Kupffer cells and blood were collected 7 days after injection. ( A ) Kupffer cell mRNA expression of IL- − 1β , TNF − α , IL − 6 , iNOS , and DPP4 was quantified by Q-PCR analysis. ( B ) Serum ALT levels were measured to assess hepatic injury. Data are presented as mean ± SEM. n = 6 mice per group. * p < 0.05, ** p < 0.01, *** p < 0.001. ALT alanine aminotransferase, AST aspartate transaminase.

Journal: International Journal of Molecular Sciences

Article Title: MyD88 Inhibition Ameliorates Diabetes-Induced Hepatic Inflammation and Gluconeogenesis Through Adipose IL-10 Induction

doi: 10.3390/ijms27062883

Figure Lengend Snippet: IL−10 injection reduces inflammatory gene expression in Kupffer cells and improves liver injury markers in Lepr db/db mice. PBS or IL−10 (10, 50, or 100 ng) was injected into adipose tissue of Lepr db/db mice. Kupffer cells and blood were collected 7 days after injection. ( A ) Kupffer cell mRNA expression of IL- − 1β , TNF − α , IL − 6 , iNOS , and DPP4 was quantified by Q-PCR analysis. ( B ) Serum ALT levels were measured to assess hepatic injury. Data are presented as mean ± SEM. n = 6 mice per group. * p < 0.05, ** p < 0.01, *** p < 0.001. ALT alanine aminotransferase, AST aspartate transaminase.

Article Snippet: Lepr db/+ mice were obtained from The Jackson Laboratory (Bar Harbor, ME, USA) and bred to generate diabetic Lepr db/db and non-diabetic Lepr +/+ mice littermates.

Techniques: Injection, Gene Expression, Expressing

IL−10 administration reduces hepatic gluconeogenic gene expression, enhances Akt activation, and improves glucose tolerance in Lepr db/db mice. PBS or IL-10 (10 or 50 ng) was injected into inguinal white adipose tissue (WAT) of Lepr db/db mice, the liver was harvested 7 days after injection and subjected to Q-PCR analysis to determine the expression of G6pc and Pck1 mRNA ( A ). ( B ) One week after injection, mice were treated with insulin (1.25 mU/g body weight) for 20 min, followed by isolation of SVFs and Western blot analysis of phosphorylated and total Akt. ( C ) Quantification of the pAkt/Akt ratio. ( D ) Glucose tolerance tests were performed by intraperitoneal glucose administration (1 g/kg body weight), with blood glucose measured at baseline and at 15 min intervals for 2 h. Data are presented as mean ± SEM. n = 4 mice per group. * p < 0.05, ** p < 0.01; # p < 0.05 compared with PBS-treated Lepr db/db mice.

Journal: International Journal of Molecular Sciences

Article Title: MyD88 Inhibition Ameliorates Diabetes-Induced Hepatic Inflammation and Gluconeogenesis Through Adipose IL-10 Induction

doi: 10.3390/ijms27062883

Figure Lengend Snippet: IL−10 administration reduces hepatic gluconeogenic gene expression, enhances Akt activation, and improves glucose tolerance in Lepr db/db mice. PBS or IL-10 (10 or 50 ng) was injected into inguinal white adipose tissue (WAT) of Lepr db/db mice, the liver was harvested 7 days after injection and subjected to Q-PCR analysis to determine the expression of G6pc and Pck1 mRNA ( A ). ( B ) One week after injection, mice were treated with insulin (1.25 mU/g body weight) for 20 min, followed by isolation of SVFs and Western blot analysis of phosphorylated and total Akt. ( C ) Quantification of the pAkt/Akt ratio. ( D ) Glucose tolerance tests were performed by intraperitoneal glucose administration (1 g/kg body weight), with blood glucose measured at baseline and at 15 min intervals for 2 h. Data are presented as mean ± SEM. n = 4 mice per group. * p < 0.05, ** p < 0.01; # p < 0.05 compared with PBS-treated Lepr db/db mice.

Article Snippet: Lepr db/+ mice were obtained from The Jackson Laboratory (Bar Harbor, ME, USA) and bred to generate diabetic Lepr db/db and non-diabetic Lepr +/+ mice littermates.

Techniques: Gene Expression, Activation Assay, Injection, Expressing, Isolation, Western Blot

( A ) For in vitro treatment, SVFs (2 × 10 7 cells) were harvested from the adipose tissue of Lepr db/db and Lepr db/db MyD88 −/− mice and treated with recombinant mouse IL-10 (10 or 100 ng) at 37 °C for 3 h. ( B ) For in vivo treatment, IL-10 (10, 50, or 100 ng) or PBS was injected into inguinal adipose tissue. After 7 days, mice were sacrificed, and liver, adipose tissue, and blood samples were collected for further analysis.

Journal: International Journal of Molecular Sciences

Article Title: MyD88 Inhibition Ameliorates Diabetes-Induced Hepatic Inflammation and Gluconeogenesis Through Adipose IL-10 Induction

doi: 10.3390/ijms27062883

Figure Lengend Snippet: ( A ) For in vitro treatment, SVFs (2 × 10 7 cells) were harvested from the adipose tissue of Lepr db/db and Lepr db/db MyD88 −/− mice and treated with recombinant mouse IL-10 (10 or 100 ng) at 37 °C for 3 h. ( B ) For in vivo treatment, IL-10 (10, 50, or 100 ng) or PBS was injected into inguinal adipose tissue. After 7 days, mice were sacrificed, and liver, adipose tissue, and blood samples were collected for further analysis.

Article Snippet: Lepr db/+ mice were obtained from The Jackson Laboratory (Bar Harbor, ME, USA) and bred to generate diabetic Lepr db/db and non-diabetic Lepr +/+ mice littermates.

Techniques: In Vitro, Recombinant, In Vivo, Injection

( A ) Genetic crosses localized mea alleles on chromosome 4. Regions definitively excluded by heterozygosity in an affected animal shown as black bars. Recombinants whose interpretation relied on penetrance in an unaffected animal are shown in grey. ( B ) PacBio HiFi reads identified a Y34X variant in mea J not present in its BKS.Cg parental strain control. ( C ) AlphaFold2 model of mouse MYSM1 shows position of the Y34X nonsense variant and the next in-frame methionine at residue 65. ( D ) Small patches of abdominal white spotting were seen on most BKS.Cg– mea J homozygotes. (E) Sanger sequencing of Mysm1 exons identified a R659G missense variant in mea 2J . (F) AlphaFold2 model shows position of the R659G variant on the surface of the catalytic MPN domain. (G) Larger patches of white spotting were typical of BKS.Cg– mea 2J homozygotes.

Journal: bioRxiv

Article Title: Mysm1 mutations in meander tail mice cause anterior-selective cerebellum malformation

doi: 10.64898/2026.02.25.708017

Figure Lengend Snippet: ( A ) Genetic crosses localized mea alleles on chromosome 4. Regions definitively excluded by heterozygosity in an affected animal shown as black bars. Recombinants whose interpretation relied on penetrance in an unaffected animal are shown in grey. ( B ) PacBio HiFi reads identified a Y34X variant in mea J not present in its BKS.Cg parental strain control. ( C ) AlphaFold2 model of mouse MYSM1 shows position of the Y34X nonsense variant and the next in-frame methionine at residue 65. ( D ) Small patches of abdominal white spotting were seen on most BKS.Cg– mea J homozygotes. (E) Sanger sequencing of Mysm1 exons identified a R659G missense variant in mea 2J . (F) AlphaFold2 model shows position of the R659G variant on the surface of the catalytic MPN domain. (G) Larger patches of white spotting were typical of BKS.Cg– mea 2J homozygotes.

Article Snippet: BKS.Cg– Dock7 m + / + Lepr db (Stock #000700), BKS.Cg– mea J Lepr db / + + (Stock #001192), and BKS.Cg– mea 2J Dock7 m / + + (Stock #001049) were obtained from live colonies and cryopreserved stocks at The Jackson Laboratories, as were mapping partner strains CAST/EiJ (Stock #000928), A/J (Stock #000646), and FVB/NJ (Stock #001800).

Techniques: Variant Assay, Control, Residue, Sequencing

( A ) Reference (Ref) and 23-bp deletion allele (D32Efs) recovered at exon 2. RNA guide sequence is underlined, with protospacer-adjacent motif shaded. Arrowhead, predicted cleavage site. Lowercase intron, uppercase exon sequences. Asterisk, T>A in mea J . ( B ) Compound mea J /Δ96 heterozygotes had shorter, kinked tails with variegated pigmentation characteristic of mea . ( C ) Classical mea alleles (from stocks carrying closely-linked Lepr db or Dock7 m mutation) and compound heterozygotes between mea J and either mea 2J or D32Efs all showed reductions in white blood cells (WBC), neutrophils (NE), lymphocytes (LY), and red blood cells (RBC), but elevated mean corpuscular volume (MCV) and mean corpuscular hemoglobin (MCH), consistent with the bone marrow failure reported for Mysm1 knockout mice. Mutants in orange, sex-matched littermate controls navy. ( D ) Midline sagittal images illustrate selective reduction of the anterior compartment (folia I-VIa, grey mask) in mea 2J , D32Efs, and compound heterozygous mutations relative to littermate controls. ( E ) Measured areas at midline showed dramatic reductions of the anterior and slight reductions in the posterior cerebellum relative to sex-matched littermates in both females (orange) and males (cyan).

Journal: bioRxiv

Article Title: Mysm1 mutations in meander tail mice cause anterior-selective cerebellum malformation

doi: 10.64898/2026.02.25.708017

Figure Lengend Snippet: ( A ) Reference (Ref) and 23-bp deletion allele (D32Efs) recovered at exon 2. RNA guide sequence is underlined, with protospacer-adjacent motif shaded. Arrowhead, predicted cleavage site. Lowercase intron, uppercase exon sequences. Asterisk, T>A in mea J . ( B ) Compound mea J /Δ96 heterozygotes had shorter, kinked tails with variegated pigmentation characteristic of mea . ( C ) Classical mea alleles (from stocks carrying closely-linked Lepr db or Dock7 m mutation) and compound heterozygotes between mea J and either mea 2J or D32Efs all showed reductions in white blood cells (WBC), neutrophils (NE), lymphocytes (LY), and red blood cells (RBC), but elevated mean corpuscular volume (MCV) and mean corpuscular hemoglobin (MCH), consistent with the bone marrow failure reported for Mysm1 knockout mice. Mutants in orange, sex-matched littermate controls navy. ( D ) Midline sagittal images illustrate selective reduction of the anterior compartment (folia I-VIa, grey mask) in mea 2J , D32Efs, and compound heterozygous mutations relative to littermate controls. ( E ) Measured areas at midline showed dramatic reductions of the anterior and slight reductions in the posterior cerebellum relative to sex-matched littermates in both females (orange) and males (cyan).

Techniques: Sequencing, Mutagenesis, Knock-Out

( A ) Amino acid sequence for mouse reference, Y34X ( mea J ), and D32Efs*13 (Δ23) alleles, showing deleted (-), termination (*), and next available in-frame AUG (M65) codons. ( B ) Comparable human reference and ClinVar alleles W51X and D92Efs relative to potential reinitiation codons at M68, M97, and M107. ( C ) Western blots of E17.5 mouse brains from control (+/+) and mutant (mut) littermate pairs for each of the three Mysm1/mea mutations using rabbit anti-MYSM1 antibody. Arrow, wild-type protein size. ( D ) Loading control on the same membrane using mouse anti-TUBG. ( E ) Dual luciferase assays using aminoterminal fusions of the fragments shown in (A) for both mouse and human MYSM1 variants plotted as log2 of the ratio of Nano luciferase to firefly luciferase. Colors denote two to three replicate transfections for each of four independent plasmid preparations. Vertical line, median of three negative controls with a frameshifted Nano luciferase.

Journal: bioRxiv

Article Title: Mysm1 mutations in meander tail mice cause anterior-selective cerebellum malformation

doi: 10.64898/2026.02.25.708017

Figure Lengend Snippet: ( A ) Amino acid sequence for mouse reference, Y34X ( mea J ), and D32Efs*13 (Δ23) alleles, showing deleted (-), termination (*), and next available in-frame AUG (M65) codons. ( B ) Comparable human reference and ClinVar alleles W51X and D92Efs relative to potential reinitiation codons at M68, M97, and M107. ( C ) Western blots of E17.5 mouse brains from control (+/+) and mutant (mut) littermate pairs for each of the three Mysm1/mea mutations using rabbit anti-MYSM1 antibody. Arrow, wild-type protein size. ( D ) Loading control on the same membrane using mouse anti-TUBG. ( E ) Dual luciferase assays using aminoterminal fusions of the fragments shown in (A) for both mouse and human MYSM1 variants plotted as log2 of the ratio of Nano luciferase to firefly luciferase. Colors denote two to three replicate transfections for each of four independent plasmid preparations. Vertical line, median of three negative controls with a frameshifted Nano luciferase.

Techniques: Sequencing, Western Blot, Control, Mutagenesis, Membrane, Luciferase, Transfection, Plasmid Preparation

(A–D) SCT-normalized mean expression of ( A ) SEMA3C and ( B ) SOX6 in human keratinocytes, and ( C ) NRP1 and ( D ) NRP2 in human endothelial cells (GSE166120). Data shown for healthy skin, diabetic skin without ulcers, healing diabetic foot ulcers, and non-healing diabetic foot ulcers. Each dot represents a sequencing run. Healthy control n = 11, diabetic non-ulcer n = 15, diabetic healing ulcer n = 9, diabetic non-healing ulcer n = 4. Statistical significance was determined using a Wilcoxon rank-sum test (p < 0.05 = *, p < 0.01 = **). ( E ) Schematic overview of the large diabetic wound ulcer model. 1-cm full-thickness wounds were generated in Lepr db /J diabetic mice before topical treatment with recombinant SEMA3C protein (human or mouse) or vehicle control at D0, D2, and D4 post-wounding. Wounds were harvested for closure and revascularization analysis at D14PW. (F–H) Representative dorsal wound images from (F) vehicle, (G) human SEMA3C , and (H) mouse Sema3c treatment groups at D4PW, D7PW, and D14PW. White dashed lines mark initial wound boundaries; yellow lines indicate wound diameter at imaging analysis. Images represent three independent biological replicates per condition (n=3). (I) Quantification of mean wound closure rate in WT and Lepr db /J mice treated with vehicle, human SEMA3C , or mouse Sema3c . Measurements taken at days D0, D2, D4, D7, D9, and D14PW. Data represents the mean of three independent biological replicates per condition (n=3), besides Lepr db /J – Vehicle which is two biological replicates. Statistical significance was determined by two-way ANOVA ( p < 0.05 = *, p < 0.01 = **). Significance is marked between Lepr db /J- mSema3c treated vs Lepr db /J – Vehicle. (J) Quantification of D7PW wound closure rate in WT and Lepr db /J mice treated with vehicle, human SEMA3C , or mouse Sema3c . Data represents the mean of three independent biological replicates per condition (n=3), besides Lepr db /J – Vehicle which is two biological replicates. Statistical significance was determined by two-way ANOVA ( p < 0.05 = *, p < 0.01 = **). (K-M) Representative ventral-view images of subcutaneous wounds in Lepr db /J mice at D14PW, treated with (K) vehicle, (L) human SEMA3C , or (M) mouse Sema3c for each condition. Boxed region highlights subcutaneous wound bed and periwound region. ( Right) Enlarged view of the boxed region. White dashed lines mark the original wound boundaries, and yellow lines indicate the central wound bed. Yellow arrowheads indicate regions with active revascularization. Images represent three independent biological replicates per condition (n=3). (N-O) Periwound revascularization coverage in Lepr db /J mice at D14PW after treatment with vehicle, human SEMA3C , or mouse Sema3c . (O) Proportion of periwound revascularization at D14PW in each treatment group. Data represents the mean of three independent biological replicates per condition (n=3). Statistical significance was determined by two-way ANOVA ( p < 0.05 = *, p < 0.01 = **). (P) Proposed model summarizing the role of the Sema3c – Nrp1/Nrp2 signaling axis in healthy versus diabetic skin wound healing. In healthy wounds, activation of Sox6 ⁺ Basal keratinocytes promote Sema3c secretion and paracrine signaling to Nrp1/Nrp2 ⁺ endothelial cells, facilitating re-epithelialization and revascularization of the wound bed. This circuit is disrupted in diabetic wounds, leading to reduced Sox6 ⁺ Basal keratinocyte activation and decreased Sema3c expression. This results in impaired re-epithelization and periwound vascular repair. However, topical reintroduction of Sema3C restores periwound revascularization and wound re-epithelization in diabetic skin ulcers.

Journal: bioRxiv

Article Title: 4D multimodal wound healing atlas reveals organ-level controls of repair phase transitions

doi: 10.64898/2026.01.15.699736

Figure Lengend Snippet: (A–D) SCT-normalized mean expression of ( A ) SEMA3C and ( B ) SOX6 in human keratinocytes, and ( C ) NRP1 and ( D ) NRP2 in human endothelial cells (GSE166120). Data shown for healthy skin, diabetic skin without ulcers, healing diabetic foot ulcers, and non-healing diabetic foot ulcers. Each dot represents a sequencing run. Healthy control n = 11, diabetic non-ulcer n = 15, diabetic healing ulcer n = 9, diabetic non-healing ulcer n = 4. Statistical significance was determined using a Wilcoxon rank-sum test (p < 0.05 = *, p < 0.01 = **). ( E ) Schematic overview of the large diabetic wound ulcer model. 1-cm full-thickness wounds were generated in Lepr db /J diabetic mice before topical treatment with recombinant SEMA3C protein (human or mouse) or vehicle control at D0, D2, and D4 post-wounding. Wounds were harvested for closure and revascularization analysis at D14PW. (F–H) Representative dorsal wound images from (F) vehicle, (G) human SEMA3C , and (H) mouse Sema3c treatment groups at D4PW, D7PW, and D14PW. White dashed lines mark initial wound boundaries; yellow lines indicate wound diameter at imaging analysis. Images represent three independent biological replicates per condition (n=3). (I) Quantification of mean wound closure rate in WT and Lepr db /J mice treated with vehicle, human SEMA3C , or mouse Sema3c . Measurements taken at days D0, D2, D4, D7, D9, and D14PW. Data represents the mean of three independent biological replicates per condition (n=3), besides Lepr db /J – Vehicle which is two biological replicates. Statistical significance was determined by two-way ANOVA ( p < 0.05 = *, p < 0.01 = **). Significance is marked between Lepr db /J- mSema3c treated vs Lepr db /J – Vehicle. (J) Quantification of D7PW wound closure rate in WT and Lepr db /J mice treated with vehicle, human SEMA3C , or mouse Sema3c . Data represents the mean of three independent biological replicates per condition (n=3), besides Lepr db /J – Vehicle which is two biological replicates. Statistical significance was determined by two-way ANOVA ( p < 0.05 = *, p < 0.01 = **). (K-M) Representative ventral-view images of subcutaneous wounds in Lepr db /J mice at D14PW, treated with (K) vehicle, (L) human SEMA3C , or (M) mouse Sema3c for each condition. Boxed region highlights subcutaneous wound bed and periwound region. ( Right) Enlarged view of the boxed region. White dashed lines mark the original wound boundaries, and yellow lines indicate the central wound bed. Yellow arrowheads indicate regions with active revascularization. Images represent three independent biological replicates per condition (n=3). (N-O) Periwound revascularization coverage in Lepr db /J mice at D14PW after treatment with vehicle, human SEMA3C , or mouse Sema3c . (O) Proportion of periwound revascularization at D14PW in each treatment group. Data represents the mean of three independent biological replicates per condition (n=3). Statistical significance was determined by two-way ANOVA ( p < 0.05 = *, p < 0.01 = **). (P) Proposed model summarizing the role of the Sema3c – Nrp1/Nrp2 signaling axis in healthy versus diabetic skin wound healing. In healthy wounds, activation of Sox6 ⁺ Basal keratinocytes promote Sema3c secretion and paracrine signaling to Nrp1/Nrp2 ⁺ endothelial cells, facilitating re-epithelialization and revascularization of the wound bed. This circuit is disrupted in diabetic wounds, leading to reduced Sox6 ⁺ Basal keratinocyte activation and decreased Sema3c expression. This results in impaired re-epithelization and periwound vascular repair. However, topical reintroduction of Sema3C restores periwound revascularization and wound re-epithelization in diabetic skin ulcers.

Article Snippet: Functional validation of the SEMA3C axis on chronic wound pathophysiology was conducted in 18-week-old Lepr db /J diabetic mice (Jackson Laboratory).

Techniques: Expressing, Sequencing, Control, Generated, Recombinant, Imaging, Activation Assay

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