STAT1 Is Required for Redifferentiation during Madin-Darby Canine Kidney Tubulogenesis

Kim, Minji; O’Brien, Lucy Erin; Kwon, Sang Ho; Mostov, Keith E.

doi:10.1091/mbc.e10-02-0112

Cited by 14 publications

(12 citation statements)

References 42 publications

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“…Cells in chains lose the apical domain, but maintain E-cadherin at the cell surface (Pollack et al 1998). Next, chains transform into cords that are 2-3 cells thick, and this transition is regulated by STAT1 (signal transducer and activator of transcription signaling) (Pollack et al 1998;Kim et al 2010). At this step, cells regain epithelial polarity and form small lumens lined by a newly established apical surface (Pollack et al 1998).…”

Section: Dynamic Rearrangements Of Polarity Drive Epithelial Morphogementioning

confidence: 99%

Polarity in Mammalian Epithelial Morphogenesis

Roignot

Peng

Mostov

2013

Cold Spring Harbor Perspectives in Biology

135

137

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SUMMARYCell polarity is fundamental for the architecture and function of epithelial tissues. Epithelial polarization requires the intervention of several fundamental cell processes, whose integration in space and time is only starting to be elucidated. To understand what governs the building of epithelial tissues during development, it is essential to consider the polarization process in the context of the whole tissue. To this end, the development of three-dimensional organotypic cell culture models has brought new insights into the mechanisms underlying the establishment and maintenance of higher-order epithelial tissue architecture, and in the dynamic remodeling of cell polarity that often occurs during development of epithelial organs. Here we discuss some important aspects of mammalian epithelial morphogenesis, from the establishment of cell polarity to epithelial tissue generation.

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Section: Dynamic Rearrangements Of Polarity Drive Epithelial Morphogementioning

confidence: 99%

Polarity in Mammalian Epithelial Morphogenesis

Roignot

Peng

Mostov

2013

Cold Spring Harbor Perspectives in Biology

135

137

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“…MDCK cysts were grown in 3D Matrigel or collagen I cultures (BD Biosciences, Sigma) (Bryant et al, 2010;Kim et al, 2010). For tubulogenesis, the Matrigel overlay was removed on day 4 by 0.25% trypsin and overlaid with collagen.…”

Section: D Cultures and Tubulogenesismentioning

confidence: 99%

“…Immunofluorescence, microscopy and image analysis Cyst or tubule were fixed and processed for immunohistochemistry as previously described (Kim et al, 2010). Primary antibodies were against: β-catenin (Santa Cruz Biotechnology, catalog number sc-7199), myosin IIA (Covance, catalog number PRB-440P), E-cadherin (BD Biosciences, catalog number 610181), ZO-1 (gift of Bruce Stevenson, Department of Cell Biology and Anatomy, University of Alberta, Canada), phosphorylated ERM (Chemicon, catalog number AB3832), PODXL (George Ojakian, Department of Anatomy and Cell Biology, State University of New York, NY), and secondary antibodies conjugated with Alexa Fluor 488 or 568 (Molecular Probes) and Hoechst 33342 (Molecular Probes) were used.…”

Section: Dna Constructs and Lentivirus Infectionmentioning

confidence: 99%

P114RhoGEF governs cell motility and lumen formation during tubulogenesis via ROCK-myosin II pathway

Kim

Shewan

Ewald

et al. 2015

Journal of Cell Science

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Tubulogenesis is fundamental to the development of many epithelial organs. Although lumen formation in cysts has received considerable attention, less is known about lumenogenesis in tubes. Here, we utilized tubulogenesis induced by hepatocyte growth factor (HGF) in MDCK cells, which form tubes enclosing a single lumen. We report the mechanism that controls tubular lumenogenesis and limits each tube to a single lumen. Knockdown of p114RhoGEF (also known as ARHGEF18), a guanine nucleotide exchange factor for RhoA, did not perturb the early stages of tubulogenesis induced by HGF. However, this knockdown impaired later stages of tubulogenesis, resulting in multiple lumens in a tube. Inhibition of Rho kinase (ROCK) or myosin IIA, which are downstream of RhoA, led to formation of multiple lumens. We studied lumen formation by live-cell imaging, which revealed that inhibition of this pathway blocked cell movement, suggesting that cell movement is necessary for consolidating multiple lumens into a single lumen. Lumen formation in tubules is mechanistically quite different from lumenogenesis in cysts. Thus, we demonstrate a new pathway that regulates directed cell migration and formation of a single lumen during epithelial tube morphogenesis.

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“…In vitro experiments with embryonic kidney explants suggested that STAT1 activation plays a pro-proliferative role in metanephric mesenchymal cells, and antagonizes epithelial differentiation and tubulogenesis 41 . Experiments with MDCK cells as a model of in vitro tubulogenesis yielded conflicting results and suggested that STAT1 is required for tubulogenesis 43 . Given that STAT1 null mice do not exhibit a defect in renal development 41 , 44 , 45 it is currently difficult to reconcile these studies or assign any definite role for STAT1 specifically in the kidney (besides its ubiquitous roles during immune responses and inflammation).…”

Section: What Is the Normal Role Of Stats In The Kidney?mentioning

confidence: 99%

Regulation of STATs by polycystin-1 and their role in polycystic kidney disease

2013

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Autosomal-dominant polycystic kidney disease (ADPKD) is a common genetic disease caused by mutations in the gene coding for polycystin-1 (PC1). PC1 can regulate STAT transcription factors by a novel, dual mechanism. STAT3 and STAT6 are aberrantly activated in renal cysts. Genetic and pharmacological approaches to inhibit STAT3 or STAT6 have led to promising results in ADPKD mouse models. Here, we review current findings that lead to a model of PC1 as a key regulator of STAT signaling in renal tubule cells. We discuss how PC1 may orchestrate appropriate epithelial responses to renal injury, and how this system may lead to aberrant STAT activation in ADPKD thereby causing inappropriate activation of tissue repair programs that culminate in renal cyst growth and fibrosis.

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STAT1 Is Required for Redifferentiation during Madin-Darby Canine Kidney Tubulogenesis

Cited by 14 publications

References 42 publications

Polarity in Mammalian Epithelial Morphogenesis

Polarity in Mammalian Epithelial Morphogenesis

P114RhoGEF governs cell motility and lumen formation during tubulogenesis via ROCK-myosin II pathway

Regulation of STATs by polycystin-1 and their role in polycystic kidney disease

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