scholarly journals The role of 3′:5′-cyclic nucleotide phosphodiesterase in regulating tissue concentrations of adenosine 3′:5′-cyclic mooophosphate

1970 ◽  
Vol 120 (4) ◽  
pp. 4P-5P
Author(s):  
J I Davies
Keyword(s):  
Cyclic Nucleotide ◽  
Cyclic Nucleotide Phosphodiesterase ◽  
Tissue Concentrations

P-264. Role of cyclic nucleotide phosphodiesterase (PDE) in GnRH secretion from GnRH neuron

1999 ◽  
Vol 14 (Suppl_3) ◽  
pp. 273-273
Author(s):  
M. Taga ◽  
H. Yoshida ◽  
H. Sakakibara ◽  
C. Ohkohchi ◽  
F. Hirahara
Keyword(s):  
Cyclic Nucleotide ◽  
Cyclic Nucleotide Phosphodiesterase ◽  
Gnrh Neuron ◽  
Gnrh Secretion

scholarly journals Cyclic nucleotide phosphodiesterase 1C contributes to abdominal aortic aneurysm

2021 ◽  
Vol 118 (31) ◽  
pp. e2107898118
Author(s):  
Chongyang Zhang ◽  
Hongmei Zhao ◽  
Yujun Cai ◽  
Jian Xiong ◽  
Amy Mohan ◽  
...  
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Cyclic Nucleotide ◽  
Aortic Aneurysms ◽  
Cyclic Nucleotide Phosphodiesterase ◽  
Causative Role ◽  
Abdominal Aortic

Abdominal aortic aneurysm (AAA) is characterized by aorta dilation due to wall degeneration, which mostly occurs in elderly males. Vascular aging is implicated in degenerative vascular pathologies, including AAA. Cyclic nucleotide phosphodiesterases, by hydrolyzing cyclic nucleotides, play critical roles in regulating vascular structure remodeling and function. Cyclic nucleotide phosphodiesterase 1C (PDE1C) expression is induced in dedifferentiated and aging vascular smooth muscle cells (SMCs), while little is known about the role of PDE1C in aneurysm. We observed that PDE1C was not expressed in normal aorta but highly induced in SMC-like cells in human and murine AAA. In mouse AAA models induced by Angiotensin II or periaortic elastase, PDE1C deficiency significantly decreased AAA incidence, aortic dilation, and elastin degradation, which supported a causative role of PDE1C in AAA development in vivo. Pharmacological inhibition of PDE1C also significantly suppressed preestablished AAA. We showed that PDE1C depletion antagonized SMC senescence in vitro and/or in vivo, as assessed by multiple senescence biomarkers, including senescence-associated β-galactosidase activity, γ-H2AX foci number, and p21 protein level. Interestingly, the role of PDE1C in SMC senescence in vitro and in vivo was dependent on Sirtuin 1 (SIRT1). Mechanistic studies further showed that cAMP derived from PDE1C inhibition stimulated SIRT1 activation, likely through a direct interaction between cAMP and SIRT1, which leads to subsequent up-regulation of SIRT1 expression. Our findings provide evidence that PDE1C elevation links SMC senescence to AAA development in both experimental animal models and human AAA, suggesting therapeutical significance of PDE1C as a potential target against aortic aneurysms.

scholarly journals Role of Ca2+/Calmodulin-Stimulated Cyclic Nucleotide Phosphodiesterase 1 in Mediating Cardiomyocyte Hypertrophy

2009 ◽  
Vol 105 (10) ◽  
pp. 956-964 ◽  
Author(s):  
Clint L. Miller ◽  
Masayoshi Oikawa ◽  
Yujun Cai ◽  
Andrew P. Wojtovich ◽  
David J. Nagel ◽  
...  
Keyword(s):  
Cyclic Nucleotide ◽  
Cyclic Nucleotide Phosphodiesterase ◽  
Cardiomyocyte Hypertrophy
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