ArticleMolecular and cellular biology2008
Retinoic acid utilizes CREB and USF1 in a transcriptional feed-forward loop in order to stimulate MKP1 expression in human immunodeficiency virus-infected podocytes.
Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 47 citations in OpenAlex.
- MAPK phosphatase 1 inhibition of p38α within lung myofibroblasts is essential for spontaneous fibrosis resolution.The Journal of clinical investigation · 2024Article
- Retinoic acid drives intestine-specific adaptation of effector ILC2s originating from distant sites.The Journal of experimental medicine · 2023Article
- USF1 modulates transcription and cellular functions by regulating multiple transcription factors in Huh7 cells.Oncology letters · 2023Article
- Nuclear receptors in podocyte biology and glomerular disease.Nature reviews. Nephrology · 2021Review
- Mitochondrial Protection by PARP Inhibition.International journal of molecular sciences · 2020Review
- Amelioration of Diabetic Nephropathy Using a Retinoic Acid ReceptorThe Journal of pharmacology and experimental therapeutics · 2018Article
- Molecular Mechanisms of Injury in HIV-Associated Nephropathy.Frontiers in medicine · 2018Review
- Protein Kinase A/CREB Signaling Prevents Adriamycin-Induced Podocyte Apoptosis via Upregulation of Mitochondrial Respiratory Chain Complexes.Molecular and cellular biology · 2018Article
- MKP-1 negative regulates Staphylococcus aureus induced inflammatory responses in Raw264.7 cells: roles of PKA-MKP-1 pathway and enhanced by rolipram.Scientific reports · 2017Article
- [Research advances in the protective effect of all-trans retinoic acid against podocyte injury].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2017Review
- Beta Interferon Production Is Regulated by p38 Mitogen-Activated Protein Kinase in Macrophages via both MSK1/2- and Tristetraprolin-Dependent Pathways.Molecular and cellular biology · 2017Article
- The podocyte as a direct target for treatment of glomerular disease?American journal of physiology. Renal physiology · 2016Review
- The beneficial role of retinoids in glomerular disease.Frontiers in medicine · 2015Review
- Interconnected network motifs control podocyte morphology and kidney function.Science signaling · 2014Article
- A new mechanism for albuminuria-induced podocyte injury.Journal of the American Society of Nephrology : JASN · 2013Article
- Calmodulin-dependent protein kinase II/cAMP response element-binding protein/Wnt/β-catenin signaling cascade regulates angiotensin II-induced podocyte injury and albuminuria.The Journal of biological chemistry · 2013Article
- Article
- SP-1 regulation of MMP-9 expression requires Ser586 in the PEST domain.The Biochemical journal · 2012Article
- Kruppel-like factor 15 (KLF15) is a key regulator of podocyte differentiation.The Journal of biological chemistry · 2012Article
- Roflumilast enhances the renal protective effects of retinoids in an HIV-1 transgenic mouse model of rapidly progressive renal failure.Kidney international · 2012Article
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Nef-induced podocyte proliferation and dedifferentiation via mitogen-activated protein kinase 1,2 (MAPK1,2) activation plays a role in human immunodeficiency virus (HIV) nephropathy pathogenesis. All-trans retinoic acid (atRA) reverses the HIV-induced podocyte phenotype by activating cyclic AMP (cAMP)/protein kinase A (PKA) and inhibiting MAPK1,2. Here we show that atRA, through cAMP and PKA, triggers a feed-forward loop involving CREB and USF1 to induce biphasic stimulation of MKP1. atRA stimulated CREB and USF1 binding to the MKP1 gene promoter, as shown by gel shifting and chromatin immunoprecipitation assays. CREB directly mediated the early phase of atRA-induced MKP1 stimulation; whereas the later phase was mediated by CREB indirectly through induction of USF1. These findings were confirmed by a reporter gene assay using the MKP1 promoter with mutation of CRE or Ebox binding sites. Consistent with these findings, the biological effects of atRA on podocytes were inhibited by silencing either MKP1, CREB, or USF1 with small interfering RNA. atRA also induced CREB phosphorylation and MKP1 expression and reduced MAPK1,2 phosphorylation in kidneys of HIV type 1-infected transgenic mice. We conclude that atRA induces sustained activation of MKP1 to suppress Nef-induced activation of the Src-MAPK1,2 pathway, thus returning the podocyte to a more differentiated state. The mechanism involves a feed-forward loop where activation of one transcription factor (TF) (CREB) leads to induction of a second TF (USF1).
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.