BIOMAT Database Logo BIOMAT Database Logo

Altered PDGF-BB-induced p38 MAP kinase activation in diabetic vascular smooth muscle cells: roles of protein kinase C-delta. 2004

Hiroshi Yamaguchi, and Masahiko Igarashi, and Akihiko Hirata, and Naoko Sugae, and Hiromi Tsuchiya, and Yumi Jimbu, and Makoto Tominaga, and Takeo Kato
Third Department of Internal Medicine, Yamagata University School of Medicine, Yamagata, Japan.

OBJECTIVE We investigated the regulation of p38 mitogen-activated protein kinase (MAPK) by platelet-derived growth factor (PDGF)-BB and its biological effects in cultured normal and diabetic rat vascular smooth muscle cells (VSMCs). RESULTS VSMC growth from diabetic rats was faster than that from normal rats. The expression of the PDGF beta-receptor in diabetic VSMCs was significantly elevated compared with that in normal cells, and PDGF-BB-induced p38 phosphorylation in diabetic cells was more enhanced via MAPK kinase (MKK) 3/6. The level of PKC activity in diabetic cells increased more than that in normal cells with or without PDGF-BB. Although protein kinase C (PKC)-betaII and PKC-delta were activated by diabetes, PDGF-BB could further enhance the level of PKC-delta alone. PDGF-BB-induced cell migration was more elevated in diabetic VSMCs, and the increase was significantly inhibited by SB-203580, rottlerin, and antisense oligodeoxynucleotides for PKC-delta. PDGF-BB-induced p38 phosphorylation also regulated cell growth, cyclooxygenase-2 levels, and arachidonic acid release, but not apoptosis. These levels were more elevated in diabetic cells, which were inhibited by SB-203580. CONCLUSIONS Our study established that PDGF-BB phosphorylated p38 via PKC-delta and the subsequent MKK 3/6, leading to cell growth regulation and the progression of a chronic inflammatory process in diabetic VSMCs.

UI MeSH Term Description Entries
D007527 Isoenzymes Structurally related forms of an enzyme. Each isoenzyme has the same mechanism and classification, but differs in its chemical, physical, or immunological characteristics. Alloenzyme,Allozyme,Isoenzyme,Isozyme,Isozymes,Alloenzymes,Allozymes
D008297 Male Males
D009131 Muscle, Smooth, Vascular The nonstriated involuntary muscle tissue of blood vessels. Vascular Smooth Muscle,Muscle, Vascular Smooth,Muscles, Vascular Smooth,Smooth Muscle, Vascular,Smooth Muscles, Vascular,Vascular Smooth Muscles
D010766 Phosphorylation The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety. Phosphorylations
D010982 Platelet-Derived Growth Factor Mitogenic peptide growth hormone carried in the alpha-granules of platelets. It is released when platelets adhere to traumatized tissues. Connective tissue cells near the traumatized region respond by initiating the process of replication. Platelet Derived Growth Factor,Factor, Platelet-Derived Growth,Growth Factor, Platelet-Derived
D011451 Prostaglandin-Endoperoxide Synthases Enzyme complexes that catalyze the formation of PROSTAGLANDINS from the appropriate unsaturated FATTY ACIDS, molecular OXYGEN, and a reduced acceptor. Fatty Acid Cyclo-Oxygenase,PGH Synthase,Prostaglandin H Synthase,Prostaglandin Synthase,Prostaglandin-Endoperoxide Synthase,Arachidonic Acid Cyclooxygenase,Cyclo-Oxygenase,Cyclooxygenase,Cyclooxygenases,Hydroperoxide Cyclase,PGH2 Synthetase,Prostaglandin Cyclo-Oxygenase,Prostaglandin Cyclooxygenase,Prostaglandin Endoperoxide Synthetase,Prostaglandin G-H Synthase,Prostaglandin H2 Synthetase,Prostaglandin Synthetase,Cyclase, Hydroperoxide,Cyclo Oxygenase,Cyclo-Oxygenase, Fatty Acid,Cyclo-Oxygenase, Prostaglandin,Cyclooxygenase, Arachidonic Acid,Cyclooxygenase, Prostaglandin,Endoperoxide Synthetase, Prostaglandin,Fatty Acid Cyclo Oxygenase,G-H Synthase, Prostaglandin,Prostaglandin Cyclo Oxygenase,Prostaglandin Endoperoxide Synthases,Prostaglandin G H Synthase,Synthase, PGH,Synthase, Prostaglandin,Synthase, Prostaglandin G-H,Synthase, Prostaglandin H,Synthase, Prostaglandin-Endoperoxide,Synthases, Prostaglandin-Endoperoxide,Synthetase, PGH2,Synthetase, Prostaglandin,Synthetase, Prostaglandin Endoperoxide,Synthetase, Prostaglandin H2
D011493 Protein Kinase C An serine-threonine protein kinase that requires the presence of physiological concentrations of CALCIUM and membrane PHOSPHOLIPIDS. The additional presence of DIACYLGLYCEROLS markedly increases its sensitivity to both calcium and phospholipids. The sensitivity of the enzyme can also be increased by PHORBOL ESTERS and it is believed that protein kinase C is the receptor protein of tumor-promoting phorbol esters. Calcium Phospholipid-Dependent Protein Kinase,Calcium-Activated Phospholipid-Dependent Kinase,PKC Serine-Threonine Kinase,Phospholipid-Sensitive Calcium-Dependent Protein Kinase,Protein Kinase M,Calcium Activated Phospholipid Dependent Kinase,Calcium Phospholipid Dependent Protein Kinase,PKC Serine Threonine Kinase,Phospholipid Sensitive Calcium Dependent Protein Kinase,Phospholipid-Dependent Kinase, Calcium-Activated,Serine-Threonine Kinase, PKC
D002465 Cell Movement The movement of cells from one location to another. Distinguish from CYTOKINESIS which is the process of dividing the CYTOPLASM of a cell. Cell Migration,Locomotion, Cell,Migration, Cell,Motility, Cell,Movement, Cell,Cell Locomotion,Cell Motility,Cell Movements,Movements, Cell
D003920 Diabetes Mellitus A heterogeneous group of disorders characterized by HYPERGLYCEMIA and GLUCOSE INTOLERANCE.
D004789 Enzyme Activation Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme. Activation, Enzyme,Activations, Enzyme,Enzyme Activations

Related Publications

Hiroshi Yamaguchi, and Masahiko Igarashi, and Akihiko Hirata, and Naoko Sugae, and Hiromi Tsuchiya, and Yumi Jimbu, and Makoto Tominaga, and Takeo Kato
AVP-induced activation of MAP kinase in vascular smooth muscle cells is mediated through protein kinase C.
October 1993, The American journal of physiology,
Hiroshi Yamaguchi, and Masahiko Igarashi, and Akihiko Hirata, and Naoko Sugae, and Hiromi Tsuchiya, and Yumi Jimbu, and Makoto Tominaga, and Takeo Kato
Activation of Inward Rectifier K+ Channel 2.1 by PDGF-BB in Rat Vascular Smooth Muscle Cells through Protein Kinase A.
January 2020, BioMed research international,
Hiroshi Yamaguchi, and Masahiko Igarashi, and Akihiko Hirata, and Naoko Sugae, and Hiromi Tsuchiya, and Yumi Jimbu, and Makoto Tominaga, and Takeo Kato
Mechanisms of inhibition by heparin of PDGF stimulated MAP kinase activation in vascular smooth muscle cells.
July 1997, Journal of cellular physiology,
Hiroshi Yamaguchi, and Masahiko Igarashi, and Akihiko Hirata, and Naoko Sugae, and Hiromi Tsuchiya, and Yumi Jimbu, and Makoto Tominaga, and Takeo Kato
Differential effects of PDGF and PDGF-BB on vascular smooth muscle cells.
May 1989, Biochemical and biophysical research communications,
Hiroshi Yamaguchi, and Masahiko Igarashi, and Akihiko Hirata, and Naoko Sugae, and Hiromi Tsuchiya, and Yumi Jimbu, and Makoto Tominaga, and Takeo Kato
Proprotein convertase PC5 regulation by PDGF-BB involves PI3-kinase/p70(s6)-kinase activation in vascular smooth muscle cells.
February 2002, Hypertension (Dallas, Tex. : 1979),
Hiroshi Yamaguchi, and Masahiko Igarashi, and Akihiko Hirata, and Naoko Sugae, and Hiromi Tsuchiya, and Yumi Jimbu, and Makoto Tominaga, and Takeo Kato
Protein kinase C inhibits insulin-induced Akt activation in vascular smooth muscle cells.
September 2001, Cellular and molecular biology (Noisy-le-Grand, France),
Hiroshi Yamaguchi, and Masahiko Igarashi, and Akihiko Hirata, and Naoko Sugae, and Hiromi Tsuchiya, and Yumi Jimbu, and Makoto Tominaga, and Takeo Kato
Distinct roles of Ca2+, calmodulin, and protein kinase C in H2O2-induced activation of ERK1/2, p38 MAPK, and protein kinase B signaling in vascular smooth muscle cells.
April 2004, Antioxidants & redox signaling,
Hiroshi Yamaguchi, and Masahiko Igarashi, and Akihiko Hirata, and Naoko Sugae, and Hiromi Tsuchiya, and Yumi Jimbu, and Makoto Tominaga, and Takeo Kato
Translocation of protein kinase C-delta by PDGF in cultured vascular smooth muscle cells: inhibition by TGF-beta 1.
January 1996, Artery,
Hiroshi Yamaguchi, and Masahiko Igarashi, and Akihiko Hirata, and Naoko Sugae, and Hiromi Tsuchiya, and Yumi Jimbu, and Makoto Tominaga, and Takeo Kato
Angiotensin II-induced activation of p21-activated kinase 1 requires Ca2+ and protein kinase C{delta} in vascular smooth muscle cells.
November 2005, American journal of physiology. Cell physiology,
Hiroshi Yamaguchi, and Masahiko Igarashi, and Akihiko Hirata, and Naoko Sugae, and Hiromi Tsuchiya, and Yumi Jimbu, and Makoto Tominaga, and Takeo Kato
Rapid activation of the novel serine/threonine protein kinase, protein kinase D by phorbol esters, angiotensin II and PDGF-BB in vascular smooth muscle cells.
May 1998, FEBS letters,
Copied contents to your clipboard!