Monocyte chemoattractant protein 1-mediated migration of mesenchymal stem cells is a source of intimal hyperplasia.

OBJECTIVE: Intimal hyperplasia is considered to be a healing response and is a major cause of vessel narrowing after injury, where migration of vascular progenitor cells contributes to pathological events, including transplant arteriosclerosis. APPROACH AND RESULTS: In this study, we used a rat aortic-allograft model to identify the predominant cell types associated with transplant arteriosclerosis and to identify factors important in their recruitment into the graft. Transplantation of labeled adventitial tissues allowed us to identify the adventitia as a major source of cells migrating to the intima. RNA microarrays revealed a potential role for monocyte chemoattractant protein 1 (MCP-1), stromal cell-derived factor 1, regulated on activation, normal T cell expressed and secreted, and interferon-inducible protein 10 in the induced vasculopathy. MCP-1 induced migration of adventitial fibroblast cells. CCR2, the receptor for MCP-1, was coexpressed with CD90, CD44, NG2, or sca-1 on mesenchymal stem cells. In vivo experiments using MCP-1-deficient and CCR2-deficient mice confirmed an important role of MCP-1 in the formation of intimal hyperplasia in a mouse model of vascular injury. CONCLUSIONS: The adventitia is a potentially important cellular source that contributes to intimal hyperplasia, and MCP-1 is a potent chemokine for the recruitment of adventitial vascular progenitor cells to intimal lesions.

Influence of Scuba Diving on the Quality of Life of People with Physical Disabilities.

The aim of the study was to assess quality of life related to mental and physical health among divers and non-divers with physical disabilities. The examined group consisted of 240 disabled people (both genders). The SF-36 questionnaire (Short-Form Health Survey) was used to measure the overall sense of health-related quality of life. Moreover, the authors' survey was also used in the study. There was a significant difference (p < 0.05) in the self-assessment of the quality of life (physical functioning, social functioning, mental health, and vitality) between the examined diving and non-diving groups. In other areas evaluated with the use of the SF-36 questionnaire, i.e., limitation in performing roles due to emotional problems and pain, limitations in performing roles due to physical health, a tendency to a higher rating was noticed in the group of divers. Scuba diving can improve various components of the life-quality of people with disabilities, and in general can be seen as a form of physical activity and rehabilitation for people with disabilities. However, it is necessary to conduct extensive research in this area.

Scuba Diving as a Form of Rehabilitation for People with Physical Disabilities.

(1) Background: The exploration of the potential therapeutic benefits of scuba diving for the mental and physical health of people with physical disabilities. (2) Methods: The research was conducted on a group of 240 people (men and women) with physical disabilities, using the survey designed by one of the authors. The subjective sense of physical and mental fitness was analyzed in retrospective and real terms. (3) Results: Significant increases in self-esteem, belief in our own abilities (self-confidence) and improvement in the ability to engage in social interactions were observed in the group of scuba divers with disabilities compared to individuals with disabilities not practicing diving. The respondents also declared an improvement in the efficiency of the respiratory system and stressed that a water environment increased their motor skills and relieved pain. (4) Conclusions: Diving can become one of the forms of rehabilitation for people with disabilities. There is a need for further research to expand our understanding of the benefits and possible health problems involved in diving. These activities have a huge impact on improving the quality of life of people with disabilities.

RCMV increases intimal hyperplasia by inducing inflammation, MCP-1 expression and recruitment of adventitial cells to intima.

BACKGROUND: Cytomegalovirus (CMV) infection has been associated with accelerated transplant vasculopathy. In this study, we assessed the effects of acute rat CMV (RCMV) infection on vessel remodeling in transplant vasculopathy, focusing on allograft morphology, inflammation and contribution of adventitial cells to intimal hyperplasia. METHODS: Infrarenal aorta was locally infected with RCMV and transplanted from female F344 rats to male Lewis rats. Graft samples were collected 2 and 8 weeks after transplantation and analyzed for intimal hyperplasia, collagen degradation and inflammation. Transplantation of aorta followed by transplantation of RCMV infected and labeled isogenic adventitia were performed to study migration of adventitial cells towards the intima. RESULTS: Intimal hyperplasia was increased threefold in infected allografts. RCMV induced apoptosis in the media, expression of matrix metalloproteinase 2, and decreased collagen deposits. Macrophage infiltration was increased in the infected allografts and resulted in increased production of MCP-1. RCMV-infected macrophages were observed in the adventitia and intima. Cells derived from infected adventitia migrated towards the intima of the allograft. CONCLUSIONS: RCMV enhances infiltration of macrophages to the allografts, and thereby increases MCP-1 production and inflammation, followed by recruitment of adventitial cells to the intima and accelerated intimal hyperplasia.

Host-derived smooth muscle cells accumulate in cardiac allografts: role of inflammation and monocyte chemoattractant protein 1.

Transplant arteriosclerosis is characterized by inflammation and intimal thickening caused by accumulation of smooth muscle cells (SMCs) both from donor and recipient. We assessed the relationship between clinical factors and the presence of host-derived SMCs in 124 myocardial biopsies from 26 consecutive patients who received hearts from opposite-sex donors. Clinical and demographic information was obtained from the patients' medical records. Host-derived SMCs accounted for 3.35+/-2.3% of cells in arterioles (range, 0.08-12.51%). As shown by linear regression analysis, an increased number of SMCs was associated with rejection grade (mean, 1.41+/-1.03, p = 0.034) and the number of leukocytes (19.1+/-12.7 per 20 high-power fields, p = 0.01). The accumulation of host-derived SMCs was associated with an increased number of leukocytes in the allografts. In vitro, monocyte chemoattractant protein 1 (MCP-1) released from leukocytes was crucial for SMC migration. After heart allotransplantation, mice treated with MCP-1-specific antibodies had significantly fewer host-derived SMCs in the grafts than mice treated with isotypic antibody controls. We conclude that the number of host-derived SMCs in human cardiac allografts is associated with the rejection grade and that MCP-1 may play pivotal role in recruiting host-derived SMCs into cardiac allografts.