Cd68 and Stabilin-1 Positive Macrophages in Postinfarction Myocardial Regeneration

Gombozhapova, A; Роговская, Ю. В.; Ребенкова, М. С.; Кжышковская, Ю. Г.; Рябов, В. В.

doi:10.15829/1560-4071-2017-11-56-61

Cited by 6 publications

(1 citation statement)

References 10 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The severity of atherosclerotic plaque infiltration by the inflammatory cells is associated with the burden of atherosclerosis, hyperproduction of a wide range of cytokines and chemokines with pro-inflammatory activities, and increases in the serum concentrations of immunological biomarkers, primarily of high sensitive C-reactive protein (hsCRP) and interleukin 6 (IL-6). These processes correlate with the worsening of atherosclerotic vascular lesion and the development of cardiovascular complications irrespective of serum concentration of lipids and confirm the key role of inflammation in atherogenesis [19,[21][22][23][24][25].…”

Section: Concepts Of Atherosclerosissupporting

confidence: 52%

Atherosclerosis. Macrophages. Viral infections

Рябов

Алексеева

Gombozhapova

et al. 2021

SMJ

Self Cite

View full text Add to dashboard Cite

The emergence of new COVID-19 infection aggravated the existing issues and gave rise to new challenges associated with the impact of viruses on the atherosclerotic process and development of cardiovascular complications. Atherosclerosis is a multifactorial disease and its progression is largely determined by dyslipidemia and chronic low-grade systemic vascular inflammation. There are a number of viruses known to be involved in maintaining the inflammatory state through the prolonged viral persistence and replication in the macrophages whose plasticity changes due to the infection. The viruses can trigger the pro-atherogenic cytokine response through the diverse macrophage-dependent mechanisms. There is lack of data regarding impact of viral infections on the monocyte/macrophage plasticity and possible control of inflammation in atherogenesis. It is still unclear whether the relationships between the viral diseases and atherosclerosis are causal or merely associative. In this review, we summarize and critically analyze the current state of knowledge regarding the virus-related mechanisms promoting atherosclerosis.

show abstract

Section: Concepts Of Atherosclerosissupporting

confidence: 52%

Atherosclerosis. Macrophages. Viral infections

Рябов

Алексеева

Gombozhapova

et al. 2021

SMJ

Self Cite

View full text Add to dashboard Cite

show abstract

The class D scavenger receptor CD68 contributes to mouse chronic liver injury

Yang

Dong

et al. 2018

Immunol Res

View full text Add to dashboard Cite

Scavenger receptors, which are expressed on monocyte/macrophages, play a central role in many pathogenic processes. Here, we examined the role of the class D scavenger receptor (CD68) in bone marrow-derived monocyte/macrophages (BMMs) in chronic liver injury. The expression pattern of multiple scavenger receptors in two liver injury models (methionine-choline-deficient and high fat (MCDHF), carbon tetrachloride (CCl)) were analyzed by qRT-PCR. CD68 expression was characterized by flow cytometric analysis, immunofluorescence, and qRT-PCR. A selective monocyte/macrophage toxicant, gadolinium chloride (GdCl) was applied to analyze the function of CD68 in vitro and in vivo. Among the seven examined scavenger receptors (CD68, CD36, CD204, MARCO, LOX1, SREC, and CD163), the mRNA expression of CD68 first got uppermost and continuously increased throughout the entire stage of chronic liver injury, thus attracting our attention. In the injured liver, the percentage of recruited CD68 BMM increased notably, aligning along the developing fibrotic septa, while the proportion of CD68 KC stayed the same compared with that of control mice. In vitro CD68 was highly expressed in primary cultured BMM, and CD68 reduction was triggered by macrophage phagocytosis and apoptosis in the presence of GdCl. In the damaged liver, the recruitment of CD68 BMM and CD68 mRNA expression were reduced by GdCl administration, leading to the attenuation of liver inflammation and fibrosis. Altogether, scavenger receptor CD68 plays a key role in mouse chronic liver injury, which has important implications for the design of anti-fibrotic therapies.

show abstract

Effect of intramyocardial allogenic biomaterial injection on angiogenesis and postischemic scar remodeling in rats

Лебедева¹,

Муслимов²,

Musina³

et al. 2020

RJTAO

View full text Add to dashboard Cite

Scar smoothing out, angiogenesis stimulation and cardiomyogenesis in myocardial infarction still remain pressing issues despite the variety of existing methods. One of the ways to correct them is intramyocardial implantation of an alloplant biomaterial (ABM) suspension. ABM serves as an inhibitor of fibroneogenesis in various tissues with chronic inflammatory processes. No studies have been carried out with regards to acute myocardial infarction. Objective: to assess the dynamics of the number of bFGF-1 + cells and CD68 macrophages, the degree of angiogenesis amidst the use of ABM in the formation of postinfarction scar in the experiment. Materials and methods. Experimental studies were performed on 100 male Wistar rats weighing 0.18–0.25 kg. Coronary artery ligation was performed on all animals. In the experimental group, the ABM suspension (12 mg) was injected intramyocardially. We used histological, electron microscopic, immunohistochemical (CD68, bFGF-1), morphometric and statistical research methods. Hearts were procured at day 3, 7, 14, 30, and 45. Results. The use of an allogeneic biomaterial immediately after coronary artery stenosis could reduce the area of cicatricial myocardial degeneration by two fold by accelerating inflammatory response and the onset of early proliferative phase. In the reactive zone after ABM implantation, macrophage myocardial infiltration significantly decreased in comparison to the control group. The use of ABM ensures significant predominance of bFGF-1+ cells in the initial period of inflammation (3–14 days). Subsequently (14–45 days), inflammatory cytokine expression became several times less, which corresponded to biodegradation and resorption of the biomaterial. In the control group, during the acute phase of inflammation (3–14 days), bFGF-1+ cells were low in number. Subsequently (14–45 days), cytokine expression increased significantly, causing rapid accumulation of collagen fibers and scarring. In myocardial regeneration after a heart attack in the experiment, ABM stimulated angiogenesis, whose level was three times higher than in the control group. It was noted that ABM serves as a regulator of the neofibrillogenesis-fibroclasia balance in tissue. Conclusion. Macrophage migration inhibition and suppression of pro-inflammatory orientation of macrophages should be indicated as one of the directions of therapeutic correction strategy for ischemic myocardial injuries. Alloplant biomaterial used in the acute phase of myocardial inflammation can serve as such alternative.

show abstract

Cd68 and Stabilin-1 Positive Macrophages in Postinfarction Myocardial Regeneration

Cited by 6 publications

References 10 publications

Atherosclerosis. Macrophages. Viral infections

Atherosclerosis. Macrophages. Viral infections

The class D scavenger receptor CD68 contributes to mouse chronic liver injury

Effect of intramyocardial allogenic biomaterial injection on angiogenesis and postischemic scar remodeling in rats

Contact Info

Product

Resources

About