Age-related changes in angiogenesis in human dermis

Гунин, А. Г.; Petrov, Vadim V.; Golubtzova, N N; Vasilieva, O. V.; Kornilova, N. K.

doi:10.1016/j.exger.2014.04.010

Cited by 63 publications

(33 citation statements)

References 31 publications

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“…In the bone marrow, resolution of infection decreased the amount of DLL4 expressed on the surface of multipotent progenitor cells. We also observed age-related changes in DLL4 expression in uninfected mice, a finding that may reflect previous research demonstrating changes in Notch ligand expression in stromal cells as a result of time in human tissues (34). We were able to verify that our antibody was specific for DLL4 using dendritic cells derived from Mx Cre Dll4 ff mice (Figure S1 in Supplementary Material).…”

Section: Resultssupporting

confidence: 88%

Systemic Expression of Notch Ligand Delta-Like 4 during Mycobacterial Infection Alters the T Cell Immune Response

et al. 2016

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The Notch ligand delta-like 4 (DLL4) is known to fine-tune the CD4+ T cell cytokine response. DLL4 is expressed on the surface of antigen-presenting cells (APCs) in a MyD88-dependent manner. We found that DLL4 expression was upregulated on bone marrow progenitor cells and APCs in mice infected with BCG Mycobacterium. Transfer of DLL4+ progenitor cells from infected hosts resulted in an increase DLL4+ myeloid cells in the spleen, indicating that expression of the dll4 gene is propagated throughout hematopoiesis. We also found an increase in DLL4+ monocytes from individuals who were infected with Mycobacterium tuberculosis. In latent individuals, DLL4 expression correlated with increased cytokine production from T cells in response to PPD stimulation. Finally, antibody blockade of DLL4 reduced T cell cytokine production from naïve T cells stimulated with antigen. These results demonstrate that the Notch ligand DLL4 can influence T cell cytokine production in both humans and mice, and further reveal that expression of DLL4 is upregulated on early hematopoietic progenitors in response to chronic mycobacterial infection. These data suggest that widespread DLL4 expression may occur as a result of mycobacterial infection, and that this expression may alter CD4+ T cell responses to both previously encountered and novel antigens.

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Section: Resultssupporting

confidence: 88%

Systemic Expression of Notch Ligand Delta-Like 4 during Mycobacterial Infection Alters the T Cell Immune Response

et al. 2016

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“…With ageing, a progressive reduction of dermis vasculature is present, due to a reduction in the number and size of vascular vessels [131]. Age-related decrease in the number of dermal blood vessels is suggested to be due to an impairment of VEGF signalling [133]. In addition, it has been reported that eNOS activity is required for full expression of reflex cutaneous vasodilation, and its impairment in aged skin is associated with alterations in NO signalling [134], increase of oxidative stress and upregulation of arginase [135].…”

Section: Introductionmentioning

confidence: 99%

Ageing and microvasculature

et al. 2014

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A decline in the function of the microvasculature occurs with ageing. An impairment of endothelial properties represents a main aspect of age-related microvascular alterations. Endothelial dysfunction manifests itself through a reduced angiogenic capacity, an aberrant expression of adhesion molecules and an impaired vasodilatory function. Increased expression of adhesion molecules amplifies the interaction with circulating factors and inflammatory cells. The latter occurs in both conduit arteries and resistance arterioles. Age-related impaired function also associates with phenotypic alterations of microvascular cells, such as endothelial cells, smooth muscle cells and pericytes. Age-related morphological changes are in most of cases organ-specific and include microvascular wall thickening and collagen deposition that affect the basement membrane, with the consequent perivascular fibrosis. Data from experimental models indicate that decreased nitric oxide (NO) bioavailability, caused by impaired eNOS activity and NO inactivation, is one of the causes responsible for age-related microvascular endothelial dysfunction. Consequently, vasodilatory responses decline with age in coronary, skeletal, cerebral and vascular beds. Several therapeutic attempts have been suggested to improve microvascular function in age-related end-organ failure, and include the classic anti-atherosclerotic and anti-ischemic treatments, and also new innovative strategies. Change of life style, antioxidant regimens and anti-inflammatory treatments gave the most promising results. Research efforts should persist to fully elucidate the biomolecular basis of age-related microvascular dysfunction in order to better support new therapeutic strategies aimed to improve quality of life and to reduce morbidity and mortality among the elderly patients.

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“…Endoneurial vasculature is required for the outgrowth of axons from the proximal stump, and angiogenesis is essential for nerve regeneration [89]. However, clinically, with increasing age, there is a reduction in, or lack of, angiogenesis in response to injury [90].…”

Section: Decreasing Recovery With Patient Agementioning

confidence: 99%

Restoration of Neurological Function Following Peripheral Nerve Trauma

Kuffler

Foy

2020

IJMS

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Following peripheral nerve trauma that damages a length of the nerve, recovery of function is generally limited. This is because no material tested for bridging nerve gaps promotes good axon regeneration across the gap under conditions associated with common nerve traumas. While many materials have been tested, sensory nerve grafts remain the clinical “gold standard” technique. This is despite the significant limitations in the conditions under which they restore function. Thus, they induce reliable and good recovery only for patients < 25 years old, when gaps are <2 cm in length, and when repairs are performed <2–3 months post trauma. Repairs performed when these values are larger result in a precipitous decrease in neurological recovery. Further, when patients have more than one parameter larger than these values, there is normally no functional recovery. Clinically, there has been little progress in developing new techniques that increase the level of functional recovery following peripheral nerve injury. This paper examines the efficacies and limitations of sensory nerve grafts and various other techniques used to induce functional neurological recovery, and how these might be improved to induce more extensive functional recovery. It also discusses preliminary data from the clinical application of a novel technique that restores neurological function across long nerve gaps, when repairs are performed at long times post-trauma, and in older patients, even under all three of these conditions. Thus, it appears that function can be restored under conditions where sensory nerve grafts are not effective.

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Age-related changes in angiogenesis in human dermis

Cited by 63 publications

References 31 publications

Systemic Expression of Notch Ligand Delta-Like 4 during Mycobacterial Infection Alters the T Cell Immune Response

Systemic Expression of Notch Ligand Delta-Like 4 during Mycobacterial Infection Alters the T Cell Immune Response

Ageing and microvasculature

Restoration of Neurological Function Following Peripheral Nerve Trauma

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