cGMP-dependent Protein Kinase Inhibits Serum-response Element-dependent Transcription by Inhibiting Rho Activation and Functions*

RhoA, in its active GTP-bound form, stimulates transcription through activation of the serum-response factor (SRF). We found that cGMP inhibited serum-induced Rho·GTP loading and transcriptional activation of SRF-dependent reporter genes in smooth muscle and glial cells in a cGMP-dependent protein kinase (G-kinase)-dependent fashion. Serum stimulation of the SRF target gene vinculin was also blocked by cGMP/G-kinase. G-kinase activation inhibited SRF-dependent transcription induced by upstream RhoA activators including Gα13 and p115RhoGEF, with Gα13-induced Rho·GTP loading inhibited by G-kinase. G-kinase had no effect on the high activation levels of RhoA(63L) or the double mutant RhoA(63L,188A) but inhibited transcriptional activation by these two RhoA mutants to a similar extent, suggesting an effect downstream of RhoA and independent of RhoA Ser188phosphorylation. Constitutively active forms of the Rho effectors Rho kinase (ROK), PKN, and PRK-2 induced SRF-dependent transcription in a cell type-specific fashion with ROK being the most efficient; G-kinase inhibited transcription induced by all three effectors without affecting ROK catalytic activity. G-kinase had no effect on RhoA(63L)-induced morphological changes in glial cells, suggesting distinct transcriptional and cytoskeletal effectors of RhoA. We conclude that G-kinase inhibits SRF-dependent transcription by interfering with RhoA signaling; G-kinase acts both upstream of RhoA, inhibiting serum- or Gα13-induced Rho activation, and downstream of RhoA, inhibiting steps distal to the Rho targets ROK, PKN, and PRK-2.

• Publication year

  2002

• Venue

  Journal of Biological Chemistry

• Publication date

  2002-10-04

• Fields of study

  Biology, Medicine, Chemistry

• Identifiers
  DOI 10.1074/jbc.M204491200PMID 12119292
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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