CCL28 contributes to angiogenesis and cardiac repair by CCR10+ endothelial cells after myocardial infarction
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PROVIDER: PRJNA1230996 | ENA |
REPOSITORIES: ENA
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Project description:Secretome-based therapies targeting angiogenesis are promising in ischemic heart disease (IHD). The effects of Chemokine C-C motif ligand (CCL) 28 on IHD remain unclear. This study investigated the role of CCL28 in angiogenesis in IHD. The myocardial infarction (MI) and hindlimb ischemia (HI) models were constructed on male wild-type and CCL28-knockout mice. AAV9-TIE1-sh-CCR10 induced endothelial specific CCR10 deficiency in mice by tail vein injection. Recombinant CCL28 protein was used to treat MI and HI in wild-type and db/db mice. Serum levels of CCL28 were evaluated in a cohort of 416 consecutive chronic total occlusions (CTO) patients. The upregulated CCL28/ C-C motif receptor (CCR)10 axis was observed in myocardial and hindlimb ischemia. Additionally, CCL28 was mainly secreted by macrophages and CCR10 was highly expressed in endothelial cells (ECs). Compared to CCR10- ECs, CCR10+ ECs exhibited robust proangiogenic capacity, which are induced by CCL28 through the CCR10/ERK/SOX5 positive feedback signaling. Deletion of CCL28 results in impaired angiogenesis in the ischemic models while the use of recombinant CCL28 protein has therapeutic potential for myocardial and hindlimb ischemia, including in diabetes. Endothelial specific CCR10 deficiency impairs angiogenesis and blocks the therapeutic effect of rCCL28 in the myocardial and hindlimb ischemia. Serum CCL28 levels exhibited the predictive effect on coronary collateral vessels (CCV) in CTO patients. CCR10+ endothelial cells (ECs) are characterized with the enhanced proangiogenic capacity and beneficial for angiogenesis. CCL28 promotes angiogenesis by increasing CCR10+ ECs via the CCR10/ERK/SOX5 positive feedback signaling. This study highlights the angiogenic role of CCL28 and recombinant CCL28 protein might be a potential therapeutic option to attenuate myocardial and hindlimb ischemia, including in diabetes.
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Project description:Four major mucosal-associated chemokines, CCL25, CCL28, CXCL14, and CXCL17, play an important role in protecting mucosal surfaces from infectious pathogens. However, their role in protection against genital herpes remains to be fully explored. The CCL28 is a chemoattractant for the CCR10 receptor-expressing immune cells and is produced homeostatically in the human vaginal mucosa (VM). In this study, we investigated the role of the CCL28/CCR10 chemokine axis in mobilizing protective antiviral B and T cell subsets into the VM site of herpes infection. We report a significant increase in the frequencies of HSV-specific memory CCR10+CD44+CD8+ T cells, expressing high levels of CCR10, in herpes-infected asymptomatic (ASYMP) women compared with symptomatic women. Similarly, a significant increase in the CCL28 chemokine (a ligand of CCR10), was detected in the VM of herpes-infected ASYMP C57BL/6 mice, associated with the mobilization of high frequencies of HSV-specific effector memory CCR10+CD44+CD62L-CD8+ TEM cells and memory CCR10+B220+CD27+ B cells in the VM of HSV-infected ASYMP mice. Inversely, compared with wild-type C57BL/6 mice, the CCL28 knockout (CCL28-/-) mice (1) appeared to be more susceptible to intravaginal infection and reinfection with HSV type 2, and (2) exhibited a significant decrease in the frequencies of HSV-specific effector memory CCR10+CD44+CD62L-CD8+ TEM cells and of memory CD27+B220+ B cells in the infected VM. These findings suggest a critical role of the CCL28/CCR10 chemokine axis in the mobilization of antiviral memory B and T cells within the VM to protect against genital herpes infection and disease.
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