Reduced Gja5 expression in arterial endothelial cells impairs arteriogenesis during acute ischemic cardiovascular disease

Lu,Xiang‑Jun; Wang,Hai‑Tao

doi:10.3892/etm.2017.5068

Reduced Gja5 expression in arterial endothelial cells impairs arteriogenesis during acute ischemic cardiovascular disease

Authors:
- Xiang‑Jun Lu
- Hai‑Tao Wang
View Affiliations

Affiliations: Radiological Department, Zhejiang Provincial People's Hospital, Hangzhou, Zhejiang 310014, P.R. China, Cardiothoracic Department, Zhejiang Provincial People's Hospital, Hangzhou, Zhejiang 310014, P.R. China
Published online on: August 30, 2017 https://doi.org/10.3892/etm.2017.5068
Pages: 4339-4343

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )

Metrics: Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )

Cited By (CrossRef): 0 citations Loading Articles...

Abstract

The aim of the present study was to investigate the functional role of gap junction protein α 5 (Gja5) in arterial endothelial cells in the arteriogenesis that occurs during acute ischemic cardiovascular disease. Gja5 knockout mice and the femoral artery occlusion (FAO) model were used in the current study. Perfusions of both hindlimbs were obtained separately prior to FAO, immediately following FAO and 1, 3, 7, 14 and 21 days after FAO using a Laser Doppler Flow Imager. Genetic evidence concerning the gastrocnemicus (GC) muscle was collected by reverse transcription‑quantitative polymerase chain reaction. There were significant reductions in the hindlimb perfusion of Gja5‑/‑ mice compared with Gja5+/+ mice 1, 3, 7, 14 and 21 days following FAO. In Gja5+/‑ and in Gja5+/+ mice, the expression of Gja5 in the GC muscle was increased 4‑fold in the ischemic hindlimb 3 days following FAO. Levels of Gja5 expression then returned to baseline values 7 days after FAO. The results of the present study demonstrated that arterial Gja5 expression serves a functional role in acute ischemic cardiovascular disease.

View Figures

View References

1	Hamawy AH, Lee LY, Crystal RG and Rosengart TK: Cardiac angiogenesis and gene therapy: A strategy for myocardial revascularization. Curr Opin Cardiol. 14:515–522. 1999. View Article : Google Scholar : PubMed/NCBI
2	Pursnani S, Korley F, Gopaul R, Kanade P, Chandra N, Shaw RE and Bangalore S: Percutaneous coronary intervention versus optimal medical therapy in stable coronary artery disease: A systematic review and meta-analysis of randomized clinical trials. Circ Cardiovasc Interv. 5:476–490. 2012. View Article : Google Scholar : PubMed/NCBI
3	Olearchyk AS: Coronary revascularization: Past, present and future. J Ukr Med Assoc North Am. 1:3–34. 1988.
4	Prior BM, Yang HT and Terjung RL: What makes vessels grow with exercise training? J Appl Physiol (1985). 97:1119–1128. 2004. View Article : Google Scholar : PubMed/NCBI
5	Carmeliet P: Mechanisms of angiogenesis and arteriogenesis. Nat Med. 6:389–395. 2000. View Article : Google Scholar : PubMed/NCBI
6	Haefliger JA, Nicod P and Meda P: Contribution of connexins to the function of the vascular wall. Cardiovasc Res. 62:345–356. 2004. View Article : Google Scholar : PubMed/NCBI
7	Ross R: Cell biology of atherosclerosis. Annu Rev Physiol. 57:791–804. 1995. View Article : Google Scholar : PubMed/NCBI
8	Lodish HF, Rodriguez RK and Klionsky DJ: Points of view: Lectures: Can't learn with them, can't learn without them. Cell Biol Educ. 3:202–211. 2004. View Article : Google Scholar : PubMed/NCBI
9	Sohl G and Willecke K: Gap junctions and the connexin protein family. Cardiovasc Res. 62:228–232. 2004. View Article : Google Scholar : PubMed/NCBI
10	Miquerol L, Meysen S, Mangoni M, Bois P, van Rijen HV, Abran P, Jongsma H, Nargeot J and Gros D: Architectural and functional asymmetry of the His-Purkinje system of the murine heart. Cardiovasc Res. 63:77–86. 2004. View Article : Google Scholar : PubMed/NCBI
11	Chadjichristos CE, Scheckenbach KE, van Veen TA, Sarieddine Richani MZ, de Wit C, Yang Z, Roth I, Bacchetta M, Viswambharan H, Foglia B, et al: Endothelial-specific deletion of connexin40 promotes atherosclerosis by increasing CD73-dependent leukocyte adhesion. Circulation. 121:123–131. 2010. View Article : Google Scholar : PubMed/NCBI
12	Chadjichristos CE, Scheckenbach KE, van Veen TA, Sarieddine Richani MZ, de Wit C, Yang Z, Roth I, Bacchetta M, Viswambharan H, Foglia B, et al: Endothelial-specific deletion of connexin40 promotes atherosclerosis by increasing CD73-dependent leukocyte adhesion. Circulation. 121:123–131. 2010. View Article : Google Scholar : PubMed/NCBI
13	Miquerol L, Meysen S, Mangoni M, Bois P, van Rijen HV, Abran P, Jongsma H, Nargeot J and Gros D: Architectural and functional asymmetry of the His-Purkinje system of the murine heart. Cardiovasc Res. 63:77–86. 2004. View Article : Google Scholar : PubMed/NCBI
14	United States Department of Agriculture (USDA): Animal Welfare Act and Animal Welfare Regulations. USDA; Washington, DC: 2013
15	Hoefer IE, van Royen N, Rectenwald JE, Deindl E, Hua J, Jost M, Grundmann S, Voskuil M, Ozaki CK, Piek JJ and Buschmann IR: Arteriogenesis proceeds via ICAM-1/Mac-1-mediated mechanisms. Circ Res. 94:1179–1185. 2004. View Article : Google Scholar : PubMed/NCBI
16	Chalothorn D, Zhang H, Clayton JA, Thomas SA and Faber JE: Catecholamines augment collateral vessel growth and angiogenesis in hindlimb ischemia. Am J Physiol Heart Circ Physiol. 289:H947–H959. 2005. View Article : Google Scholar : PubMed/NCBI
17	Jakobsson A and Nilsson GE: Prediction of sampling depth and photon pathlength in laser Doppler flowmetry. Med Biol Eng Comput. 31:301–307. 1993. View Article : Google Scholar : PubMed/NCBI
18	Chalothorn D, Clayton JA, Zhang H, Pomp D and Faber JE: Collateral density, remodeling, and VEGF-A expression differ widely between mouse strains. Physiol Genomics. 30:179–191. 2007. View Article : Google Scholar : PubMed/NCBI
19	Helisch A, Wagner S, Khan N, Drinane M, Wolfram S, Heil M, Ziegelhoeffer T, Brandt U, Pearlman JD, Swartz HM and Schaper W: Impact of mouse strain differences in innate hindlimb collateral vasculature. Arterioscler Thromb Vasc Biol. 26:520–526. 2006. View Article : Google Scholar : PubMed/NCBI
20	Carmen, Schoninger Olaf, Wieser A.A. Ghermanan, et al: Anatomy. 2th. New Emperor Publishing Ltd.; Klagenfurt: pp. 122–125. 2001, (In German).
21	van Oostrom MC, van Oostrom O, Quax PH, Verhaar MC and Hoefer IE: Insights into mechanisms behind arteriogenesis: What does the future hold? J Leukoc Biol. 84:1379–1391. 2008. View Article : Google Scholar : PubMed/NCBI
22	Buschmann I and Schaper W: The pathophysiology of the collareral circulation (arteriogenesis). J Pathol. 190:338–342. 2000. View Article : Google Scholar : PubMed/NCBI
23	Schaper W: Collateral circulation: Past and present. Basic Res Cardiol. 104:5–21. 2009. View Article : Google Scholar : PubMed/NCBI
24	Heil M and Schaper W: Influence of mechanical, cellular, and molecular factors on collateral artery growth (arteriogenesis). Circ Res. 95:449–458. 2004. View Article : Google Scholar : PubMed/NCBI
25	Heil M, Eitenmüller I, Schmitz-Rixen T and Schaper W: Arteriogenesis versus angiogenesis: Similarities and differences. J Cell Mol Med. 10:45–55. 2006. View Article : Google Scholar : PubMed/NCBI
26	Buschmann I and Schaper W: Arteriogenesis versus angiogenesis: Two mechanisms of vessel growth. News Physiol Sci. 14:121–125. 1999.PubMed/NCBI
27	Söhl G and Willecke K: Gap junctions and the connexin protein family. Cardiovasc Res. 62:228–232. 2004. View Article : Google Scholar : PubMed/NCBI
28	Carmeliet P and Tessier-Lavigne M: Common mechanisms of nerve and blood vessel wiring. Nature. 436:193–200. 2005. View Article : Google Scholar : PubMed/NCBI
29	Pipp F, Boehm S, Cai WJ, Adili F, Ziegler B, Karanovic G, Ritter R, Balzer J, Scheler C, Schaper W and Schmitz-Rixen T: Elevated fluid shear stress enhances postocclusive collateral artery growth and gene expression in the pig hindlimb. Arterioscler Thromb Vasc Biol. 24:1664–1668. 2004. View Article : Google Scholar : PubMed/NCBI