ArticleThe Journal of clinical investigation2015
SDF1 induction by acidosis from principal cells regulates intercalated cell subtype distribution.
Article in The Journal of clinical investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Intercalated cell function, kidney innate immunity, and urinary tract infections.Pflugers Archiv : European journal of physiology · 2024Review
- The pathophysiology of distal renal tubular acidosis.Nature reviews. Nephrology · 2023Review
- The proximal tubule through an NBCe1-dependent mechanism regulates collecting duct phenotypic and remodeling responses to acidosis.American journal of physiology. Renal physiology · 2023Article
- Ammonium chloride-induced acidosis exacerbates cystitis and pyelonephritis caused by uropathogenic E. coli.Physiological reports · 2022Article
- Lipopolysaccharide directly inhibits bicarbonate absorption by the renal outer medullary collecting duct.Scientific reports · 2020Article
- Metabolic acidosis exacerbates pyelonephritis in mice prone to vesicoureteral reflux.Physiological reports · 2020Article
- Adaptive response of the murine collecting duct to alkali loading.Pflugers Archiv : European journal of physiology · 2020Article
- Screening and function discussion of a hereditary renal tubular acidosis family pathogenic gene.Cell death & disease · 2020Article
- Acidosis induces antimicrobial peptide expression and resistance to uropathogenicAmerican journal of physiology. Renal physiology · 2020Article
- Synergy Between Low Dose Metronomic Chemotherapy and the pH-centered Approach Against Cancer.International journal of molecular sciences · 2019Review
- Vasopressin Increases Urinary AcidificationJournal of the American Society of Nephrology : JASN · 2019Article
- CAIX furthers tumour progression in the hypoxic tumour microenvironment of esophageal carcinoma and is a possible therapeutic target.Journal of enzyme inhibition and medicinal chemistry · 2018Article
- Pathophysiology, diagnosis and treatment of inherited distal renal tubular acidosis.Journal of nephrology · 2018Review
- Improving outcomes for patients with distal renal tubular acidosis: recent advances and challenges ahead.Pediatric health, medicine and therapeutics · 2018Review
- Metabolic acidosis stimulates the production of the antimicrobial peptide cathelicidin in rabbit urine.American journal of physiology. Renal physiology · 2017Article
- Transcription factoreLife · 2017Article
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Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
Abstract
The nephron cortical collecting duct (CCD) is composed of principal cells, which mediate Na, K, and water transport, and intercalated cells (ICs), which are specialized for acid-base transport. There are two canonical IC forms: acid-secreting α-ICs and HCO3-secreting β-ICs. Chronic acidosis increases α-ICs at the expense of β-ICs, thereby increasing net acid secretion by the CCD. We found by growth factor quantitative PCR array that acidosis increases expression of mRNA encoding SDF1 (or CXCL12) in kidney cortex and isolated CCDs from mouse and rabbit kidney cortex. Exogenous SDF1 or pH 6.8 media increased H+ secretion and decreased HCO3 secretion in isolated perfused rabbit CCDs. Acid-dependent changes in H+ and HCO3 secretion were largely blunted by AMD3100, which selectively blocks the SDF1 receptor CXCR4. In mice, diet-induced chronic acidosis increased α-ICs and decreased β-ICs. Additionally, IC-specific Cxcr4 deletion prevented IC subtype alterations and magnified metabolic acidosis. SDF1 was transcriptionally regulated and a target of the hypoxia-sensing transcription factor HIF1α. IC-specific deletion of Hif1a produced no effect on mice fed an acid diet, as α-ICs increased and β-ICs decreased similarly to that observed in WT littermates. However, Hif1a deletion in all CCD cells prevented acidosis-induced IC subtype distribution, resulting in more severe acidosis. Cultured principal cells exhibited an HIF1α-dependent increase of Sdf1 transcription in response to media acidification. Thus, our results indicate that principal cells respond to acid by producing SDF1, which then acts on adjacent ICs.
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