scholarly journals The polycystin-1 C-terminal fragment triggers branching morphogenesis and migration of tubular kidney epithelial cells

2002 ◽  
Vol 109 (4) ◽  
pp. 481-489 ◽  
Author(s):  
Christian Nickel ◽  
Thomas Benzing ◽  
Lorenz Sellin ◽  
Peter Gerke ◽  
Anil Karihaloo ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Branching Morphogenesis ◽  
Terminal Fragment ◽  
Kidney Epithelial Cells ◽  
And Migration

scholarly journals Polycystin-2 Regulates Proliferation and Branching Morphogenesis in Kidney Epithelial Cells

2005 ◽  
Vol 281 (1) ◽  
pp. 137-144 ◽  
Author(s):  
David H. Grimm ◽  
Anil Karihaloo ◽  
Yiqiang Cai ◽  
Stefan Somlo ◽  
Lloyd G. Cantley ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Branching Morphogenesis ◽  
Kidney Epithelial Cells

scholarly journals Motogenic and morphogenic activity of epithelial receptor tyrosine kinases.

1996 ◽  
Vol 133 (5) ◽  
pp. 1095-1107 ◽  
Author(s):  
M Sachs ◽  
K M Weidner ◽  
V Brinkmann ◽  
I Walther ◽  
A Obermeier ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cell Motility ◽  
Tyrosine Kinases ◽  
Receptor Tyrosine Kinases ◽  
Mutational Analysis ◽  
Three Dimensional ◽  
Branching Morphogenesis ◽  
Met Receptor ◽  
Kidney Epithelial Cells

Receptor tyrosine kinases play essential roles in morphogenesis and differentiation of epithelia. Here we examined various tyrosine kinase receptors, which are preferentially expressed in epithelia (c-met, c-ros, c-neu, and the keratin growth factor [KGF] receptor), for their capacity to induce cell motility and branching morphogenesis of epithelial cells. We exchanged the ligand-binding domain of these receptors by the ectodomain of trkA and could thus control signaling by the new ligand, NGF. We demonstrate here that the tyrosine kinases of c-met, c-ros, c-neu, the KGF receptor, and trkA, but not the insulin receptor, induced scattering and increased motility of kidney epithelial cells in tissue culture. Mutational analysis suggests that SHC binding is essential for scattering and increased cell motility induced by trkA. The induction of motility in epithelial cells is thus an important feature of various receptor tyrosine kinases, which in vivo play a role in embryogenesis and metastasis. In contrast, only the c-met receptor promoted branching morphogenesis of kidney epithelial cells in three-dimensional matrices, which resemble the formation of tubular epithelia in development. Interestingly, the ability of c-met to induce morphogenesis could be transferred to trkA, when in a novel receptor hybrid COOH-terminal sequences of c-met (including Y14 to Y16) were fused to the trkA kinase domain. These data demonstrate that tubulogenesis of epithelia is a restricted activity of tyrosine kinases, as yet only demonstrated for the c-met receptor. We predict the existence of specific substrates that mediate this morphogenesis signal.

scholarly journals Effect of Slit/Robo signaling on regeneration in lung emphysema

2021 ◽  
Author(s):  
Jin-Soo Park ◽  
RyeonJin Cho ◽  
Eun-Young Kang ◽  
Yeon-Mok Oh
Keyword(s):  
Epithelial Cells ◽  
Mouse Model ◽  
Lung Epithelial Cells ◽  
Mouse Lung ◽  
Chronic Obstructive ◽  
Irreversible Damage ◽  
Lung Epithelial ◽  
And Migration ◽  
Proliferation And Migration

AbstractEmphysema, a pathological component of chronic obstructive pulmonary disease, causes irreversible damage to the lung. Previous studies have shown that Slit plays essential roles in cell proliferation, angiogenesis, and organ development. In this study, we evaluated the effect of Slit2 on the proliferation and migration of mouse lung epithelial cells and its role in regeneration in an emphysema lung mouse model. Here, we have shown that Slit2/Robo signaling contributes to the regeneration of lungs damaged by emphysema. Mouse epithelial lung cells treated with Slit2 exhibited increased proliferation and migration in vitro. Our results also showed that Slit2 administration improved alveolar regeneration in the emphysema mouse model in vivo. Furthermore, Slit2/Robo signaling increased the phosphorylation of ERK and Akt, which was mediated by Ras activity. These Slit2-mediated cellular signaling processes may be involved in the proliferation and migration of mouse lung epithelial cells and are also associated with the potential mechanism of lung regeneration. Our findings suggest that Slit2 administration may be beneficial for alveolar regeneration in lungs damaged by emphysema.

scholarly journals Effects of bone morphogenetic proteins on epithelial repair

2021 ◽  
pp. 153537022110281
Author(s):  
Yu Hou ◽  
Yu-Xi He ◽  
Jia-Hao Zhang ◽  
Shu-Rong Wang ◽  
Yan Zhang
Keyword(s):  
Growth Factors ◽  
Epithelial Cells ◽  
Bone Morphogenetic Proteins ◽  
Epithelial Tissue ◽  
Epithelial Repair ◽  
Multiple Functions ◽  
Epithelial Damage ◽  
Damage Repair ◽  
And Migration ◽  
Proliferation And Migration

Epithelial tissue has important functions such as protection, secretion, and sensation. Epithelial damage is involved in various pathological processes. Bone morphogenetic proteins (BMPs) are a class of growth factors with multiple functions. They play important roles in epithelial cells, including in differentiation, proliferation, and migration during the repair of the epithelium. This article reviews the functions and mechanisms of the most profoundly studied BMPs in the process of epithelial damage repair and their clinical significance.

Aberrant responses to growth-regulatory signals by variant kidney epithelial cells

1988 ◽  
Vol 254 (5) ◽  
pp. F747-F753
Author(s):  
M. M. Walsh-Reitz ◽  
R. I. Feldman ◽  
F. G. Toback
Keyword(s):  
Epithelial Cells ◽  
Growth Regulation ◽  
Growth Inhibitor ◽  
Soft Agar ◽  
Isoenzyme Analysis ◽  
Variant Cell ◽  
Kidney Epithelial Cells ◽  
Potent Growth ◽  
Potent Growth Inhibitor ◽  
Low K

Cultures that achieved a higher cell density than expected were noted during study of growth regulation in monkey kidney epithelial cells of the BSC-1 line. Multiplication of the variant cells was accelerated, compared with parental cells, as the cultures approached confluence. Cytogenetic analysis, immunofluorescence antibody reactions with specific monkey serum, isoenzyme analysis, microbiological studies, and lack of growth in soft agar indicated that the variant cells were not a contaminating cell type, lacked new isoenzymes, were free of microbial contamination, and were not transformed. Confluent variant cultures did not respond to a purified growth inhibitor protein produced by BSC-1 cells that inhibits multiplication and reduces cell Na content in subconfluent variant and parental cells. Vasopressin, which is a mitogen for parental cells, was a potent growth inhibitor for confluent cultures of variant cells. Low-K or high-Na media, which stimulate proliferation of parental cells, had no effect on growth of the variant cell line. These results suggest that enhanced multiplication of the variant cells is mediated by altered signal transduction pathways and/or receptors for growth-regulatory molecules.

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