2. Academic Validation
  3. RSAD2 is abundant in atherosclerotic plaques and promotes interferon-induced CXCR3-chemokines in human smooth muscle cells

RSAD2 is abundant in atherosclerotic plaques and promotes interferon-induced CXCR3-chemokines in human smooth muscle cells

  • Sci Rep. 2024 Apr 8;14(1):8196. doi: 10.1038/s41598-024-58592-9.
Assim Hayderi 1,  Ashok K Kumawat 2,  Vladimir S Shavva 3,  Mats Dreifaldt 2 4,  Birgitta Sigvant 5 6,  Marcelo H Petri 2 4,  Björn Kragsterman 5 7,  Peder S Olofsson 3 8,  Allan Sirsjö 2,  Liza U Ljungberg 2
Affiliations

Affiliations

  • 1 School of Medical Sciences, Örebro University, Örebro, Sweden. assim.hayderi@hotmail.com.
  • 2 School of Medical Sciences, Örebro University, Örebro, Sweden.
  • 3 Laboratory of Immunobiology, Division of Cardiovascular Medicine, Department of Medicine, Center for Bioelectronic Medicine, Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
  • 4 Department of Cardiothoracic Surgery and Vascular Surgery, Örebro University Hospital, Örebro, Sweden.
  • 5 Department of Surgical Sciences, Uppsala University, Uppsala, Sweden.
  • 6 Centre for Clinical Research and Education, Region Värmland, Karlstad, Sweden.
  • 7 Department of Surgery, Västmanlands Hospital Västerås, Västerås, Sweden.
  • 8 Institute of Bioelectronic Medicine, Feinstein Institutes for Medical Research, Manhasset, NY, USA.
PMID: 38589444 DOI: 10.1038/s41598-024-58592-9
Abstract

In atherosclerotic lesions, monocyte-derived macrophages are major source of interferon gamma (IFN-γ), a pleotropic cytokine known to regulate the expression of numerous genes, including the Antiviral gene RSAD2. While RSAD2 was reported to be expressed in endothelial cells of human carotid lesions, its significance for the development of atherosclerosis remains utterly unknown. Here, we harnessed publicly available human carotid atherosclerotic data to explore RSAD2 in lesions and employed siRNA-mediated gene-knockdown to investigate its function in IFN-γ-stimulated human aortic smooth muscle cells (hAoSMCs). Silencing RSAD2 in IFN-γ-stimulated hAoSMCs resulted in reduced expression and secretion of key CXCR3-chemokines, CXCL9, CXCL10, and CXCL11. Conditioned medium from RSAD2-deficient hAoSMCs exhibited diminished monocyte attraction in vitro compared to conditioned medium from control cells. Furthermore, RSAD2 transcript was elevated in carotid lesions where it was expressed by several different cell types, including endothelial cells, macrophages and smooth muscle cells. Interestingly, RSAD2 displayed significant correlations with CXCL10 (r = 0.45, p = 0.010) and CXCL11 (r = 0.53, p = 0.002) in human carotid lesions. Combining our findings, we uncover a novel role for RSAD2 in hAoSMCs, which could potentially contribute to monocyte recruitment in the context of atherosclerosis.

Figures
Products
嗨！很高兴为您提供帮助！

尊敬的 MCE 客户您好，
请您选择所在区域，我们将转接对应客服为您服务！

热门区域

A

B

C

F

G

H

J

L

N

Q

S

T

X

Y

Z

热 A B C F G H J L N Q S T X Y Z