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Segmental analysis of sodium transporters and claudins along the nephron in claudin‐3 knockout mice under normal sodium intake. Wild‐type (WT) and claudin‐3 knockout (Claudin‐3 KO) mice were maintained on a normal‐sodium diet (0.18% Na + ; NSD). (A) Representative Western blots showing the expression of the Na + /H + exchanger 3 <t>(NHE3),</t> the Na + –K + –2Cl − cotransporter (NKCC2), the thiazide‐sensitive sodium‐chloride cotransporter (NCC), full‐length and cleaved forms of the α‐ and γ‐subunits of the epithelial sodium channel (ENaC), β‐ENaC, pendrin, and tight junction claudins (claudin‐2, claudin‐3, claudin‐4, claudin‐7, claudin‐8, and claudin‐10) in the renal cortex of wild‐type and claudin‐3 knockout mice. (B) Densitometric quantification of protein abundance normalized to E‐cadherin from at least five animals per group. Statistical analysis was performed using the Mann–Whitney U ‐test. Data are presented as mean ± SD. kDa: kilodaltons; OD: optical density.
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Segmental analysis of sodium transporters and claudins along the nephron in claudin‐3 knockout mice under normal sodium intake. Wild‐type (WT) and claudin‐3 knockout (Claudin‐3 KO) mice were maintained on a normal‐sodium diet (0.18% Na + ; NSD). (A) Representative Western blots showing the expression of the Na + /H + exchanger 3 <t>(NHE3),</t> the Na + –K + –2Cl − cotransporter (NKCC2), the thiazide‐sensitive sodium‐chloride cotransporter (NCC), full‐length and cleaved forms of the α‐ and γ‐subunits of the epithelial sodium channel (ENaC), β‐ENaC, pendrin, and tight junction claudins (claudin‐2, claudin‐3, claudin‐4, claudin‐7, claudin‐8, and claudin‐10) in the renal cortex of wild‐type and claudin‐3 knockout mice. (B) Densitometric quantification of protein abundance normalized to E‐cadherin from at least five animals per group. Statistical analysis was performed using the Mann–Whitney U ‐test. Data are presented as mean ± SD. kDa: kilodaltons; OD: optical density.
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Segmental analysis of sodium transporters and claudins along the nephron in claudin‐3 knockout mice under normal sodium intake. Wild‐type (WT) and claudin‐3 knockout (Claudin‐3 KO) mice were maintained on a normal‐sodium diet (0.18% Na + ; NSD). (A) Representative Western blots showing the expression of the Na + /H + exchanger 3 <t>(NHE3),</t> the Na + –K + –2Cl − cotransporter (NKCC2), the thiazide‐sensitive sodium‐chloride cotransporter (NCC), full‐length and cleaved forms of the α‐ and γ‐subunits of the epithelial sodium channel (ENaC), β‐ENaC, pendrin, and tight junction claudins (claudin‐2, claudin‐3, claudin‐4, claudin‐7, claudin‐8, and claudin‐10) in the renal cortex of wild‐type and claudin‐3 knockout mice. (B) Densitometric quantification of protein abundance normalized to E‐cadherin from at least five animals per group. Statistical analysis was performed using the Mann–Whitney U ‐test. Data are presented as mean ± SD. kDa: kilodaltons; OD: optical density.
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Segmental analysis of sodium transporters and claudins along the nephron in claudin‐3 knockout mice under normal sodium intake. Wild‐type (WT) and claudin‐3 knockout (Claudin‐3 KO) mice were maintained on a normal‐sodium diet (0.18% Na + ; NSD). (A) Representative Western blots showing the expression of the Na + /H + exchanger 3 (NHE3), the Na + –K + –2Cl − cotransporter (NKCC2), the thiazide‐sensitive sodium‐chloride cotransporter (NCC), full‐length and cleaved forms of the α‐ and γ‐subunits of the epithelial sodium channel (ENaC), β‐ENaC, pendrin, and tight junction claudins (claudin‐2, claudin‐3, claudin‐4, claudin‐7, claudin‐8, and claudin‐10) in the renal cortex of wild‐type and claudin‐3 knockout mice. (B) Densitometric quantification of protein abundance normalized to E‐cadherin from at least five animals per group. Statistical analysis was performed using the Mann–Whitney U ‐test. Data are presented as mean ± SD. kDa: kilodaltons; OD: optical density.

Journal: Acta Physiologica (Oxford, England)

Article Title: Low‐Salt Diet Induces Claudin‐3 Expression and Drives Adaptive Changes in Collecting Duct of Claudin‐3‐Deficient Mice

doi: 10.1111/apha.70216

Figure Lengend Snippet: Segmental analysis of sodium transporters and claudins along the nephron in claudin‐3 knockout mice under normal sodium intake. Wild‐type (WT) and claudin‐3 knockout (Claudin‐3 KO) mice were maintained on a normal‐sodium diet (0.18% Na + ; NSD). (A) Representative Western blots showing the expression of the Na + /H + exchanger 3 (NHE3), the Na + –K + –2Cl − cotransporter (NKCC2), the thiazide‐sensitive sodium‐chloride cotransporter (NCC), full‐length and cleaved forms of the α‐ and γ‐subunits of the epithelial sodium channel (ENaC), β‐ENaC, pendrin, and tight junction claudins (claudin‐2, claudin‐3, claudin‐4, claudin‐7, claudin‐8, and claudin‐10) in the renal cortex of wild‐type and claudin‐3 knockout mice. (B) Densitometric quantification of protein abundance normalized to E‐cadherin from at least five animals per group. Statistical analysis was performed using the Mann–Whitney U ‐test. Data are presented as mean ± SD. kDa: kilodaltons; OD: optical density.

Article Snippet: NHE3 , Mouse , 1/500 , , StressMarq , SPC‐400.

Techniques: Knock-Out, Western Blot, Expressing, Quantitative Proteomics, MANN-WHITNEY