Rho-ROCK Signal Pathway Regulates Microtubule-Based Process Formation of Cultured Podocytes – Inhibition of ROCK Promoted Process Elongation

@article{Gao2004RhoROCKSP,
  title={Rho-ROCK Signal Pathway Regulates Microtubule-Based Process Formation of Cultured Podocytes – Inhibition of ROCK Promoted Process Elongation},
  author={Shuang-yan Gao and Chun-yu Li and Jie Chen and Lei Pan and Shouichiro Saito and Takehiro Terashita and Kyoko Saito and Kyojy Miyawaki and Kazuhiro Shigemoto and Katsumi Mominoki and Seiji Matsuda and Naoto Kobayashi},
  journal={Nephron Experimental Nephrology},
  year={2004},
  volume={97},
  pages={e49 - e61}
}
Background: Podocytes, renal glomerular visceral epithelial cells, have two kinds of processes, namely major processes containing microtubules (MTs) and foot processes with actin filaments (AFs). The present study investigated how MTs are organized by the Rho-ROCK signal transduction pathway during process formation of podocytes. Method: After induction of differentiation, podocytes of the conditionally immortalized mouse cell line were treated with Y-27632, a specific inhibitor of ROCK, and… 
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Rac1 Contributes to Actin Organization in Glomerular Podocytes
TLDR
Rac1 likely contributes to lamellipodia formation in differentiating MP and may contribute to process formation in podocytes recovering from injuries, and nephrin potentiates Rac1 activation.
Rho-family small GTPases are involved in forskolin-induced cell-cell contact formation of renal glomerular podocytes in vitro
TLDR
Transmission electron microscopy and the immunostaining of cell adhesion molecules and actin-associated proteins have revealed a structural change at the site of cell-cell contact following forskolin treatment, which promotes the assembly ofcell-cell contacts between podocytes via a mechanism that probably involves Rho-family small GTPases.
Rho kinase inhibitors stimulate the migration of human cultured osteoblastic cells by regulating actomyosin activity
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In the improved motility assay used in the present study, Y-27632 and HA-1077 significantly increased the migration of both osteoblasts and osteosarcoma cells on plastic in a dose-dependent and reversible manner.
Process formation of the renal glomerular podocyte: Is there common molecular machinery for processes of podocytes and neurons?
TLDR
Concerning the formation of podocyte foot processes and dendritic branches, actin filaments are thought to play a central role in orchestrating the function of various molecules and the regulation of actin assembly is necessary to establish and maintain such sophisticated cellular architecture.
Activation of RhoA in podocytes induces focal segmental glomerulosclerosis.
TLDR
Transgenic mice that express a constitutively active form of RhoA in a podocyte-specific and doxycycline-inducible manner are generated and activation of RHoA in podocytes leads to albuminuria accompanied by a range of histologic changes characteristic of minimal change disease and FSGS in humans.
Role of Rho-GTPases and their regulatory proteins in glomerular podocyte function.
TLDR
This review summarizes the recent discoveries of the molecular mechanisms by which the actin cytoskeleton is regulated in podocytes, with a particular focus on the role of the Rho-family of small GTPases, represented by RhoA, Rac1, and Cdc42.
Role of Rho-GTPases in complement-mediated glomerular epithelial cell injury.
TLDR
Exposure of GEC to complement alters the balance of RhoA, Rac1, and Cdc42 activities, which may contribute to foot process effacement and increase the resistance of G EC to complement-mediated injury.
Regulation of cofilin phosphorylation in glomerular podocytes by testis specific kinase 1 (TESK1)
TLDR
Inhibition of ROK with Y27632 failed to attenuate albuminuria or FP effacement in V14Rho mice, and TESK1 regulates podocyte cytoskeletal dynamics in glomerular podocytes and may play an important role in regulatingglomerular filtration barrier integrity in glomersular disease processes.
Over-expressing transient receptor potential cation channel 6 in podocytes induces cytoskeleton rearrangement through increases of intracellular Ca2+ and RhoA activation
TLDR
Podocytes over-expressing TRPC6 may lead to higher intracellular Ca2+ ion concentration in the presence of stimuli, which down-regulates the expression of two important molecules, nephrin on slit diaphragm and synaptopodin in cytoskeleton, and stimulates RhoA activity, which in turn causes F-actin derangement and the decrease of foot processes.
Rho-kinase inhibition prevents proteinuria in immune-complex-mediated antipodocyte nephritis.
TLDR
Data suggest that increased Rho-kinase activity in the podocyte may be a mechanism for in vivo podocyte foot process retraction in rats with passive Heymann nephritis and human kidney biopsies from patients with membranous nephropathy.
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