Literature DB >> 28649129

C33(S), a novel PDE9A inhibitor, protects against rat cardiac hypertrophy through upregulating cGMP signaling.

Pan-Xia Wang1, Zhuo-Ming Li1, Si-Dong Cai1, Jing-Yan Li1, Ping He1, Yi Huang1, Guo-Shuai Feng1, Hai-Bin Luo2, Shao-Rui Chen1, Pei-Qing Liu1.   

Abstract

Phosphodiesterase-9A (PDE9A) expression is upregulated during cardiac hypertrophy and heart failure. Accumulating evidence suggests that PDE9A might be a promising therapeutic target for heart diseases. The present study sought to investigate the effects and underlying mechanisms of C33(S), a novel selective PDE9A inhibitor, on cardiac hypertrophy in vitro and in vivo. Treatment of neonatal rat cardiomyocytes (NRCMs) with PE (100 μmol/L) or ISO (1 μmol/L) induced cardiac hypertrophy characterized by significantly increased cell surface areas and increased expression of fetal genes (ANF and BNP). Furthermore, PE or ISO significantly increased the expression of PDE9A in the cells; whereas knockdown of PDE9A significantly alleviated PE-induced hypertrophic responses. Moreover, pretreatment with PDE9A inhibitor C33(S) (50 and 500 nmol/L) or PF-7943 (2 μmol/L) also alleviated the cardiac hypertrophic responses in PE-treated NRCMs. Abdominal aortic constriction (AAC)-induced cardiac hypertrophy and ISO-induced heart failure were established in SD rats. In ISO-treated rats, oral administration of C33(S) (9, 3, and 1 mg·kg-1·d-1, for 3 consecutive weeks) significantly increased fractional shortening (43.55%±3.98%, 54.79%±1.95%, 43.98%±7.96% vs 32.18%±6.28%), ejection fraction (72.97%±4.64%, 84.29%±1.56%, 73.41%±9.37% vs 49.17%±4.20%) and cardiac output (60.01±9.11, 69.40±11.63, 58.08±8.47 mL/min vs 48.97±2.11 mL/min) but decreased the left ventricular internal diameter, suggesting that the transition to heart failure was postponed by C33(S). We further revealed that C33(S) significantly elevated intracellular cGMP levels, phosphorylation of phospholamban (PLB) and expression of SERCA2a in PE-treated NRCMs in vitro and in ISO-induced heart failure model in vivo. Our results demonstrate that C33(S) effectively protects against cardiac hypertrophy and postpones the transition to heart failure, suggesting that it is a promising agent in the treatment of cardiac diseases.

Entities:  

Mesh:

Substances:

Year:  2017        PMID: 28649129      PMCID: PMC5589968          DOI: 10.1038/aps.2017.38

Source DB:  PubMed          Journal:  Acta Pharmacol Sin        ISSN: 1671-4083            Impact factor:   6.150


  56 in total

1.  Cardiac Structure and Function in Elite Para-cyclists with Spinal Cord Injury.

Authors:  Jonathan H Kim; Jennifer L Trilk; Ryan Smith; Irfan Asif; Paul Tim Maddux; Yi-An Ko; Michael S Emery
Journal:  Med Sci Sports Exerc       Date:  2016-08       Impact factor: 5.411

2.  Tumor suppressor gene ING3 induces cardiomyocyte hypertrophy via inhibition of AMPK and activation of p38 MAPK signaling.

Authors:  Jiaojiao Wang; Zhiping Liu; Xiaojun Feng; Si Gao; Suowen Xu; Peiqing Liu
Journal:  Arch Biochem Biophys       Date:  2014-08-20       Impact factor: 4.013

3.  Cellular basis of angiotensin-(1-7)-induced augmentation of left ventricular functional performance in heart failure.

Authors:  Xiaowei Zhang; Heng-Jie Cheng; Peng Zhou; Dalane W Kitzman; Carlos M Ferrario; Wei-Min Li; Che Ping Cheng
Journal:  Int J Cardiol       Date:  2017-01-10       Impact factor: 4.164

4.  Diminished basal phosphorylation level of phospholamban in the postinfarction remodeled rat ventricle: role of beta-adrenergic pathway, G(i) protein, phosphodiesterase, and phosphatases.

Authors:  B Huang; S Wang; D Qin; M Boutjdir; N El-Sherif
Journal:  Circ Res       Date:  1999-10-29       Impact factor: 17.367

5.  cGMP/PKG pathway mediates myocardial postconditioning protection in rat hearts by delaying normalization of intracellular acidosis during reperfusion.

Authors:  Javier Inserte; Ignasi Barba; Marcos Poncelas-Nozal; Victor Hernando; Luís Agulló; Marisol Ruiz-Meana; David Garcia-Dorado
Journal:  J Mol Cell Cardiol       Date:  2011-02-26       Impact factor: 5.000

6.  Roles of cGMP-dependent protein kinase I (cGKI) and PDE5 in the regulation of Ang II-induced cardiac hypertrophy and fibrosis.

Authors:  Enrico Patrucco; Katrin Domes; Mauro Sbroggió; Anne Blaich; Jens Schlossmann; Matthias Desch; Sergei D Rybalkin; Joseph A Beavo; Robert Lukowski; Franz Hofmann
Journal:  Proc Natl Acad Sci U S A       Date:  2014-08-19       Impact factor: 11.205

7.  Neonatal gene transfer of Serca2a delays onset of hypertrophic remodeling and improves function in familial hypertrophic cardiomyopathy.

Authors:  James R Peña; Ariani C Szkudlarek; Chad M Warren; Lynley S Heinrich; Robert D Gaffin; Ganapathy Jagatheesan; Federica del Monte; Roger J Hajjar; Paul H Goldspink; R John Solaro; David F Wieczorek; Beata M Wolska
Journal:  J Mol Cell Cardiol       Date:  2010-09-18       Impact factor: 5.000

Review 8.  The alpha1-adrenergic receptors in cardiac hypertrophy: signaling mechanisms and functional implications.

Authors:  Susanna Cotecchia; Cosmo Damiano Del Vescovo; Matilde Colella; Stefania Caso; Dario Diviani
Journal:  Cell Signal       Date:  2015-07-10       Impact factor: 4.315

9.  Effect of phosphodiesterase-5 inhibition on exercise capacity and clinical status in heart failure with preserved ejection fraction: a randomized clinical trial.

Authors:  Margaret M Redfield; Horng H Chen; Barry A Borlaug; Marc J Semigran; Kerry L Lee; Gregory Lewis; Martin M LeWinter; Jean L Rouleau; David A Bull; Douglas L Mann; Anita Deswal; Lynne W Stevenson; Michael M Givertz; Elizabeth O Ofili; Christopher M O'Connor; G Michael Felker; Steven R Goldsmith; Bradley A Bart; Steven E McNulty; Jenny C Ibarra; Grace Lin; Jae K Oh; Manesh R Patel; Raymond J Kim; Russell P Tracy; Eric J Velazquez; Kevin J Anstrom; Adrian F Hernandez; Alice M Mascette; Eugene Braunwald
Journal:  JAMA       Date:  2013-03-27       Impact factor: 56.272

10.  TSH inhibits SERCA2a and the PKA/PLN pathway in rat cardiomyocytes.

Authors:  Jiajia Dong; Cuixia Gao; Jing Liu; Yunshan Cao; Limin Tian
Journal:  Oncotarget       Date:  2016-06-28
View more
  6 in total

1.  Phosphodiesterase 9 Inhibition in Models of Heart Failure With Preserved Left Ventricular Ejection Fraction: Should We Focus on the Positive or Negative?

Authors:  Robert M Blanton
Journal:  Circ Heart Fail       Date:  2020-05-18       Impact factor: 8.790

2.  Phosphodiesterase 9a Inhibition in Mouse Models of Diastolic Dysfunction.

Authors:  Mei Methawasin; Joshua Strom; Tomasz Borkowski; Zaynab Hourani; Ray Runyan; John E Smith; Henk Granzier
Journal:  Circ Heart Fail       Date:  2020-05-18       Impact factor: 8.790

3.  CRD-733, a Novel PDE9 (Phosphodiesterase 9) Inhibitor, Reverses Pressure Overload-Induced Heart Failure.

Authors:  Daniel A Richards; Mark J Aronovitz; Peiwen Liu; Gregory L Martin; Kelly Tam; Suchita Pande; Richard H Karas; Daniel M Bloomfield; Michael E Mendelsohn; Robert M Blanton
Journal:  Circ Heart Fail       Date:  2021-01-19       Impact factor: 8.790

4.  Evaluation of phosphodiesterase 9A as a novel biomarker in heart failure with preserved ejection fraction.

Authors:  Christian Besler; Karl-Philipp Rommel; Karl-Patrik Kresoja; Justus Mörbitz; Holger Kirsten; Markus Scholz; Karin Klingel; Joachim Thiery; Ralph Burkhardt; Petra Büttner; Volker Adams; Holger Thiele; Philipp Lurz
Journal:  ESC Heart Fail       Date:  2021-03-30

Review 5.  cGMP Signaling and Modulation in Heart Failure.

Authors:  Robert M Blanton
Journal:  J Cardiovasc Pharmacol       Date:  2020-05       Impact factor: 3.271

6.  Epigenome-wide association study on asthma and chronic obstructive pulmonary disease overlap reveals aberrant DNA methylations related to clinical phenotypes.

Authors:  Yung-Che Chen; Ying-Huang Tsai; Chin-Chou Wang; Shih-Feng Liu; Ting-Wen Chen; Wen-Feng Fang; Chiu-Ping Lee; Po-Yuan Hsu; Tung-Ying Chao; Chao-Chien Wu; Yu-Feng Wei; Huang-Chih Chang; Chia-Cheng Tsen; Yu-Ping Chang; Meng-Chih Lin
Journal:  Sci Rep       Date:  2021-03-03       Impact factor: 4.379

  6 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.