Journal: Scientific Reports

Article Title: Single-cell RNA sequencing revealed the association between proximal tubular epithelial cells and renal interstitial cells in chronic kidney disease progression

doi: 10.1038/s41598-025-28988-2

Figure Lengend Snippet: Renal histopathology and functional changes in adenine-induced CKD mice. A Representative images of PAS, Masson, and Sirius staining. All images are shown at identical magnification, ×200, scale bar = 50 μm. B-D Quantitative analysis of tubular injury and fibrosis. E Serum creatinine levels. F Blood urea nitrogen levels. G Representative Western blot images of FN, Col-IV, Col-I, Vimentin, and α-SMA expression in the kidneys of mice in all groups. The original blots are presented in Supplementary Fig. 1. H-L Densitometric analysis of FN, Col-IV, Col-I, Vimentin, and α-SMA normalized to α-Tubulin content. Data are expressed as mean ± SEM, n = 3. * p < 0.05, ** p < 0.01, and *** p < 0.001 compared with indicated group, ns = no significance.

Article Snippet: The evaluation of serum creatinine (Scr) and blood urea nitrogen (BUN) were measured by Creatinine Serum Detection Kit and Blood Urea Nitrogen Detection Kit (StressMarq Biosciences, British Columbia, Canada), respectively.

Techniques: Histopathology, Functional Assay, Staining, Western Blot, Expressing

Journal: Journal of Cell Communication and Signaling

Article Title: Tri‐domain proteins 27 alleviates ischemia‐reperfusion injury‐induced acute kidney injury by promoting Gli‐like transcription factor 1 expression via the inhibition of polycomb repressive complex 2 activity

doi: 10.1002/ccs3.70046

Figure Lengend Snippet: TRIM27 was significantly downregulated in the kidney tissues of I/R‐induced AKI mice and H 2 O 2 ‐treated mRTECs. An animal model of RIRI‐induced AKI was established using IRI. (A–B) Pathological changes in the kidney were analyzed by HE and PAS staining, and the injury score is presented. (C) Serum creatinine and BUN levels were examined using the corresponding kits. (D–E) Protein levels of Pax‐2, Vimentin, EED, EZH2, SUZ12, H3K27me3, and TRIM27 in the kidney tissues were determined by western blotting. A renal tubular epithelial cell injury model was established by H 2 O 2 treatment. (F) The CCK‐8 assay was used to assess mRTEC viability. (G) TRIM27, EED, EZH2, SUZ12, and H3K27me3 protein levels in the cells were examined by western blotting. N = 6. * p < 0.05, ** p < 0.01, and *** p < 0.001. AKI, acute kidney injury; BUN, blood urea nitrogen; CCK‐8, cell counting kit‐8; EED, Embryonic Ectoderm Development; EZH2, Enhancer of zeste homolog 2; H3K27me3, Histone H3 trimethylated at lysine 27; HE, hematoxylin–eosin; mRTECs, mouse renal tubular epithelial cells; PAS, periodic acid–Schiff; RIRI, renal ischemia‐reperfusion (I/R) injury; SUZ12, Suppressor of Zeste 12; TRIM27, tri‐domain proteins 27.

Article Snippet: Serum creatinine (Scr) and blood urea nitrogen (BUN) levels were measured using kits purchased from StressMarq Biosciences (#SKT‐217, #SKT‐213).

Techniques: Animal Model, Staining, Western Blot, CCK-8 Assay, Cell Counting

Journal: Journal of Cell Communication and Signaling

Article Title: Tri‐domain proteins 27 alleviates ischemia‐reperfusion injury‐induced acute kidney injury by promoting Gli‐like transcription factor 1 expression via the inhibition of polycomb repressive complex 2 activity

doi: 10.1002/ccs3.70046

Figure Lengend Snippet: TRIM27 overexpression ameliorated I/R‐induced AKI in mice. An animal model was established using I/R combined with Oe‐TRIM27 injection. (A, B) Hematoxylin and eosin (HE) and periodic acid–Schiff (PAS) staining were performed to analyze the pathological changes in the kidneys. (C) Apoptosis in the kidney tissues was analyzed by TUNEL staining. (D) Serum creatinine and BUN levels were measured using the corresponding kits. (E–F) Western blot was employed to detect TRIM27, EED, EZH2, SUZ12, GLIS1, H3K27me3, Histone H3, Pax‐2, Vimentin, and β‐catenin protein levels in kidney tissues. N = 6. * p < 0.05, ** p < 0.01, and *** p < 0.001. AKI, acute kidney injury; BUN, blood urea nitrogen; EED, Embryonic Ectoderm Development; EZH2, Enhancer of zeste homolog 2; H3K27me3, Histone H3 trimethylated at lysine 27; HE, hematoxylin and eosin; I/R, ischemia‐reperfusion; PAS, periodic acid–Schiff; SUZ12, Suppressor of Zeste 12; TRIM27, tri‐domain proteins 27; TUNEL, terminal deoxynucleotidyl transferase‐mediated dUTP nick‐end labeling.

Article Snippet: Serum creatinine (Scr) and blood urea nitrogen (BUN) levels were measured using kits purchased from StressMarq Biosciences (#SKT‐217, #SKT‐213).

Techniques: Over Expression, Animal Model, Injection, Staining, TUNEL Assay, Western Blot, End Labeling

Journal: The Kaohsiung Journal of Medical Sciences

Article Title: GATA1 Transcriptionally Upregulates LMCD1 , Promoting Ferroptosis in Sepsis‐Associated Acute Kidney Injury Through the Hippo/ YAP Pathway

doi: 10.1002/kjm2.70071

Figure Lengend Snippet: LMCD1 knockdown alleviated CLP‐induced SA‐AKI in mice. SA‐AKI mice were established using CLP and injected with AAV‐LMCD1. (A) Serum creatinine and BUN levels were examined using ELISA. (B‐D) Hematoxylin and eosin (HE) and periodic acid‐Schiff (PAS) staining were performed to analyze the pathological changes in the kidney, and the renal tubular injury score is presented. (E, F) LMCD1 expression levels were determined using qRT‐PCR and western blotting. (G‐I) ROS, MDA, GSH, SOD, and Fe 2+ levels in the kidney tissues were analyzed using appropriate kits. (J) SLC7A11, GPX4, ACSL4, Nrf2, p‐YAP, and YAP protein levels in kidney tissues were detected using western blotting. n = 6. * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Serum levels of serum creatinine (Scr), blood urea nitrogen (BUN), and LPS were determined using kits purchased from StressMarq Biosciences (BC, Canada; #SKT‐217, #SKT‐213, #SKT‐210).

Techniques: Knockdown, Injection, Enzyme-linked Immunosorbent Assay, Staining, Expressing, Quantitative RT-PCR, Western Blot