Journal: Stem cell research & therapy

Article Title: Placental mesenchymal stem cells of fetal and maternal origins demonstrate different therapeutic potentials.

doi: 10.1186/scrt436

Figure Lengend Snippet: Figure 4 Fetal P-MSCs (fPMSCs) stimulated angiogenesis in vitro in HGF-dependent manner. (A) Tube formation by HUVECs cultured in P-MSCs medium, P-MSCs medium supplemented with 20 ng/mL rhHGF, maternal P-MSCs conditioned medium (mPMSCs cM), fetal P-MSCs conditioned medium (fPMSCs cM) and fPMSCs cM plus100 ng/mL anti-HGF antibody, respectively. Images are representatives of nine randomly chosen images for each culture condition (100x magnification). (B) The average number of tube structures formed in each group as counted from nine randomly chosen images under 40x magnification. **: P <0.01. HGF, hepatocyte growth factor; HUVECs, human umbilical vein endothelial cells; P-MSCs, placental mesenchymal stem cells; rhHGF, recombinant human growth factor.

Article Snippet: Single cell suspensions were prepared in P-MSCs medium, P-MSCs medium plus 20 ng/ml recombinant human growth factor (rhHGF) (R&D System), maternal P-MSC-conditioned medium, fetal P-MSC-conditioned medium, and fetal P-MSCconditioned medium plus 100 ng/ml anti-human HGF antibody (R&D System).

Techniques: In Vitro, Cell Culture, Recombinant

Journal: Cell reports

Article Title: Pituitary adenomas evade apoptosis via noxa deregulation in Cushing’s disease

doi: 10.1016/j.celrep.2022.111223

Figure Lengend Snippet: (A) A sublabial transsphenoidal approach was used for resection of microadenomas (white arrowheads) in patients with Cushing’s disease (CD). Coronal, post-gadolinium contrast enhanced magnetic resonance image from patient P1. Adenoma and adjacent normal pituitary gland were separately annotated during surgery and dissociated into a single-cell suspension, followed by GEM embedding, sequencing, and computational analysis. Scale bar: 2 cm. (B) Summary of demographic data and analysis for patients included in the study. (C) UMAP embedding of cells from the 6 patient samples with CD, GH, NFPA, and PRL adenomas used in scRNA-seq analysis. Cells cluster according to dominant secretory phenotype. (D) UMAP embedding showing the cell-type identities cells from the 6 patient samples. (E) UMAP embedding showing CD sample identity for cells from patients P1, P2, and P3. (F) UMAP plot showing CD patient cells clustering by cell-type identity. Cell types: leukocytes (Les), endothelial cells (ECs), pericytes (Pes), folliculostellate cells (FSs), corticotrophs (Cs), gonadotroph (Gs), somatotrophs (Ss), lactotrophs (Ls), ambiguous/somato-lactotrophs (SLs), and POU1F1 -positive, hormone-negative (P + H − ) cells. GH, growth hormone; NFPA, non-functioning pituitary adenoma; PRL, prolactinoma.

Article Snippet: GH1 , Novus Biologicals , Cat #NBP2–53262.

Techniques: Suspension, Sequencing

Journal: Cell reports

Article Title: Pituitary adenomas evade apoptosis via noxa deregulation in Cushing’s disease

doi: 10.1016/j.celrep.2022.111223

Figure Lengend Snippet: (A) The UMAP plot from split by patient (top, P1; middle, P2; bottom, P3), colored by cell type. (B) Dot plot showing the expression (marker color) and percentage of cells expressing (marker size) for the top 6 cell-type upregulated genes with highest min.logFC.detected from a filtered group of robustly upregulated cell-type marker genes . Genes used as a priori known classification marker genes are indicated by bold font. (C) Multiplexed immunohistochemistry of tissue from P3, showing localization of key hormone markers in margin and core regions of the sample. White bar: 100 μm. PC, pituitary cells; HPC, hormone-producing cells; Mar, tumor margin; POMC, pro-opiomelanocortin; GH, growth hormone; PRL, prolactin; LH, luteinizing hormone; FSH, follicle-stimulating hormone.

Article Snippet: GH1 , Novus Biologicals , Cat #NBP2–53262.

Techniques: Expressing, Marker, Immunohistochemistry

Journal: Cell reports

Article Title: Pituitary adenomas evade apoptosis via noxa deregulation in Cushing’s disease

doi: 10.1016/j.celrep.2022.111223

Figure Lengend Snippet: (A) UMAP plot demonstrating PMAIP1 abundance in CD adenomas (C) but not in PRL, G, or NFPA adenomas. PMAIP1 was also detected at lower levels in Les and ECs. (B) UMAP plot showing MYC upregulation in CD corticotrophs but not other hormone-producing cells (left panel). MYC expression was also detected in Pes, ECs, and Les. Middle panel: UMAP plot showing overlap of MYC and PMAIP1 expression is mostly limited to CD corticotrophs (yellow dots). Right panel: UMAP plot showing UCHL1 abundance in most hormone-producing cell types in CD. (C) Bulk RNA-seq of CD and non-CD samples verified overexpression of pro-apoptotic genes including PMAIP1 in CD tissues. (D) DNA methylation levels (beta values) at CpG sites associated with the PMAIP1 promoter methylation demonstrating hypomethylation in CD (n = 3) compared with normal (autopsy-derived, n = 20) pituitary glands. *p < 0.05. (E) Multiplex immunohistochemistry (mIHC) of 5 μm thick sections from a CD adenoma. Insets from the core-margin boundary represented by white dashed lines. White bar: 100 μm. Core-margin boundary identified by overlaying expression of POMC, TBX19, and DAPI. Compared with the margin, core adenoma cells show robust overexpression of POMC, TBX19, and MYC; however, noxa expression is decreased within the adenoma core. (F) Representative image from noxa IHC in independent adenoma/normal pairs (n = 10). Pairwise analysis of noxa deconvoluted IHC images (absorbance = mean pixel intensity count per pixel) showing suppressed noxa signal in CD adenomas compared with normal (margin) tissues (p = 0.0013; 95% confidence interval [CI] −0.027 to −0.007). Scale bar: 100 μM. (G) Expected epithelial growth factor (EGF) signaling upregulation and ERK1/2 phosphorylation were found in human CD adenoma primary cell lines (P6_CD and P26_CD). A, adenoma (core); N, normal (margin) pituitary gland. Noxa was undetectable or decreased in core adenomas. (H) A survey of human primary CD adenoma cell lines revealed variable noxa expression compared with sCD adenoma, GH adenoma, and NFPA. CD, corticotroph adenoma causing Cushing’s disease; sCD, hormonally silent corticotroph adenoma; GH, growth-hormone-secreting adenoma; NFPA, non-functioning pituitary adenoma.

Article Snippet: GH1 , Novus Biologicals , Cat #NBP2–53262.

Techniques: Expressing, RNA Sequencing, Over Expression, DNA Methylation Assay, Methylation, Derivative Assay, Multiplex Assay, Immunohistochemistry, Phospho-proteomics

Journal: Cell reports

Article Title: Pituitary adenomas evade apoptosis via noxa deregulation in Cushing’s disease

doi: 10.1016/j.celrep.2022.111223

Figure Lengend Snippet: KEY RESOURCES TABLE

Article Snippet: GH1 , Novus Biologicals , Cat #NBP2–53262.

Techniques: Recombinant, Enzyme-linked Immunosorbent Assay, Sequencing

Journal: Cell Reports Medicine

Article Title: Unacylated-Ghrelin Impairs Hippocampal Neurogenesis and Memory in Mice and Is Altered in Parkinson’s Dementia in Humans

doi: 10.1016/j.xcrm.2020.100120

Figure Lengend Snippet:

Article Snippet: For IGF-1 and GH, platelet-rich plasma samples were analyzed using Human IGF-1 DuoSet ELISA (cat. No. DY291, R&D Systems), and Human GH DuoSet ELISA (Cat. No. DY1067, R&D Systems), using half-volume Nunclon Microwell 96-well plates.

Techniques: Clinical Proteomics, Recombinant, Saline, RNAscope, Bicinchoninic Acid Protein Assay, Enzyme-linked Immunosorbent Assay, Software, Microscopy