b6 dba  (Jackson Laboratory)

Journal: Journal of nephrology

Article Title: Phenotypic quantification of Nphs1-deficient mice

doi: 10.1007/s40620-024-01987-8

Figure Lengend Snippet: Validation of nephrin deficiency in Nphs1 knockout (KO) mouse model and Kaplan–Meier survival analysis. A Upper panel shows representative immunofluorescence images of coronal equatorial kidney sections of wildtype C57BL/6 mouse (P28). Glomerular podocytes are marked by WT1 signal (red) and show positive NPHS1 expression (green). Nuclei are marked by DAPI staining (blue). B Lower panel show representative immunofluorescence images of coronal equatorial kidney sections of Nphs1 KO mouse model ( Nphs1 fl/fl NPHS2-Cre + ) at P28. Glomerular podocytes are marked by WT1 (red) but lack NPHS1 expression. Nuclei are stained by DAPI. C Nphs1 fl/fl NPHS2-Cre + mice have significantly lower median survival age compared to the controls. Mice were evaluated until the age of 50 days. In total, 74 mice were evaluated consisting of Nphs1 fl/fl NPHS2-Cre + mice ( n = 27) with a median survival age of 5 days compared with two control groups: Nphs1 fl/ + NPHS2-Cre + mice ( n = 30) and Nphs1 +/+ NPHS2-Cre + mice ( n = 17). log-rank (Mantel-Cox) test, **** P < 0.0001; log-rank test for trend, **** P < 0.0001; Gehan-Breslow-Wilcoxon test, **** P < 0.0001

Article Snippet: We acquired a nephrin-floxed mouse model B6(DBA)- Nphs1 tm1Afrn /J (JAX Stock No. 027824 from the Jackson Laboratory) that was previously studied for metabolic pathways linked to pancreatic β -cell survival, however, was never studied for any renal phenotype.

Techniques: Biomarker Discovery, Knock-Out, Immunofluorescence, Expressing, Staining, Control

Journal: Journal of nephrology

Article Title: Phenotypic quantification of Nphs1-deficient mice

doi: 10.1007/s40620-024-01987-8

Figure Lengend Snippet: Quantification of tubular microcysts and glomerular cysts in Nphs1 fl/fl NPHS2-Cre + mice and littermate controls upon light torial kidney sections of 6 microscopy. A , B Representative image of PAS-stained coronal equa- Nphs1 fl/f NPHS2-Cre + ( Nphs1 KO) and 6 control mice ( Nphs1 fl/ + NPHS2-Cre + or Nphs1 fl/ + NPHS2-Cre- ) that were imaged and evaluated according to the following standardized steps: 1. identify the cortex (*), outer medulla (**), inner medulla (***), and kidney papilla (black arrow), 2. determine “standard critical surface area” (SCSA) by measuring the diameter of an equatorial section of a mature glomerulus (encircled by a black line in enlargement of ( B ), and 3. count the number of tubular structures with a diameter exceeding half the SCSA diameter (arrowheads in enlargement of ( B ). Furthermore, sections were then evaluated for glomerular cysts (red arrow in enlargement of ( B ). C Nphs1 KO mice had a median of 85 tubular microcysts per section ( n = 6), whereas control mice had a median of 2.5 microcysts per kidney section ( n = 6). Unpaired t-test, **** P < 0.0001. D Evaluation Nphs1 KO mice kidney sections revealed a median of 8.5 glomerular microcysts ( n = 6), whereas the median for Nphs1 fl/ + NPHS2-Cre + control mice was 0 ( n = 6). Unpaired t -test, **** P < 0.0001

Article Snippet: We acquired a nephrin-floxed mouse model B6(DBA)- Nphs1 tm1Afrn /J (JAX Stock No. 027824 from the Jackson Laboratory) that was previously studied for metabolic pathways linked to pancreatic β -cell survival, however, was never studied for any renal phenotype.

Techniques: Microscopy, Staining, Control

Journal: Journal of nephrology

Article Title: Phenotypic quantification of Nphs1-deficient mice

doi: 10.1007/s40620-024-01987-8

Figure Lengend Snippet: Transmission electron microscopy (TEM) analysis and quantification of podocyte foot process (PFP) per μm of GBM length. A Representative image from a heterozygous Nphs1 fl/ + NPHS2 − Cre + mouse with multiple PFP. B A representative image from a homozygous Nphs1 fl/fl NPHS2 − Cre + mouse ( Nphs1 KO) with severe tertiary PFP effacement. To establish quantification of PFP effacement, a GBM within a glomerulus was identified and included in the analysis if the laminae ( rara interna, densa, and rara externa ) were symmetric and the adjacent endothelial fenestrae rhythmic (blue arrow), indicating a perpendicular section of the GBM. A yellow line was then drawn along the GBM in ImageJ for as long as these criteria were met. Then the number of PFP (red arrowheads) was counted along the yellow line. C Nphs1 fl/ + NPHS2-Cre + or Nphs1 fl/ + NPHS2-Cre- control mice ( n = 11) (green bars) showed a mean of 2.35 tertiary foot processes (FP) per tuft length [μm] in comparison to Nphs1 fl/fl NPHS2 − Cre + mice ( Nphs1 KO) ( n = 8) (red bars) which showed a mean of 0.77 FP/μm. The X-axis positions relate to individual mice. Each dot/square represents a separate evaluated TEM image of the same mouse. (from C ) as measured in the control mice and D Pooled numbers of PFP per μm of GBM length Nphs1fl/fl NPHS2 − Cre + KO mice. Unpaired t -test, ****, P < 0.0001

Article Snippet: We acquired a nephrin-floxed mouse model B6(DBA)- Nphs1 tm1Afrn /J (JAX Stock No. 027824 from the Jackson Laboratory) that was previously studied for metabolic pathways linked to pancreatic β -cell survival, however, was never studied for any renal phenotype.

Techniques: Transmission Assay, Electron Microscopy, Control, Comparison

Journal: Journal of nephrology

Article Title: Phenotypic quantification of Nphs1-deficient mice

doi: 10.1007/s40620-024-01987-8

Figure Lengend Snippet: Urine albumin to creatinine ratios in KO mice and littermate controls. A Nphs1 fl/fl NPHS2 − Cre + mice developed significant and early albuminuria (red curves, n = 10) vs . healthy littermate controls (blue). Black hatches represent the median level of urine albumin to creatinine ratio at every time point. B Mean urine albumin to creatinine ratios over time are depicted for Nphs1 fl/fl . NPHS2 − Cre + ( Nphs1 KO) and healthy littermate controls. Unpaired t -test, **** P < 0.0001

Article Snippet: We acquired a nephrin-floxed mouse model B6(DBA)- Nphs1 tm1Afrn /J (JAX Stock No. 027824 from the Jackson Laboratory) that was previously studied for metabolic pathways linked to pancreatic β -cell survival, however, was never studied for any renal phenotype.

Techniques:

Journal: The Journal of Physiology

Article Title: An α7 nicotinic and GABA B receptor‐mediated pathway controls acetylcholine release in the tripartite neuromuscular junction

doi: 10.1113/JP287243

Figure Lengend Snippet: Differential expressions of genes of interest.

Article Snippet: To delete Chrna7, we used a floxed allele of Chrna7 ((B6;DBA(Cg)‐Chrna7tm1.1Ehs/YakelJ) in which exon4 of the α7 nAChRs gene is flanked by LoxP recognized by the recombinase Cre (JAX stock #026965; The Jackson Laboratory, Bar Harbor, ME, USA) (Hernandez et al., ).

Techniques: