View attachment 22569new hairs come in slowly and they are strong like zondas. lol
if it keeps comming like that i will have a pagani hairline. lol/.
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i am telling you all if hair comes back and stays i have it all.
View attachment 22571
ahahhahahahahaha!
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Thrombospondin-1 plays a critical role in the induction of hair follicle involution and vascular regression during the catagen phase.
Yano K,
Brown LF,
Lawler J,
Miyakawa T,
Detmar M.
Source
Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, USA.
Abstract
Hair growth is associated with pronounced vascular-endothelial-growth-factor-induced perifollicular angiogenesis, whereas the catagen regression phase is characterized by apoptosis-driven blood vessel regression. The biologic relevance of endogenous inhibitors of angiogenesis in the control of hair cycling, however, has remained unknown. We studied the expression and biologic role of the angiogenesis inhibitor thrombospondin-1 (TSP-1) during the induced adult hair follicle cycle in wild-type, TSP-1 deficient, and TSP-1 overexpressing transgenic mice. TSP-1 expression was absent from hair bulb and dermal papilla cells during early to mid-anagen but was highly upregulated throughout the catagen involution phase. In TSP-1 deficient mice, the follicle growth phase was significantly prolonged, associated with increased perifollicular vascularization and vascular proliferation. Conversely, hair follicle growth was delayed in K14/TSP-1 transgenic mice that expressed high levels of TSP-1 in outer root sheath keratinocytes, associated with reduced perifollicular vascularization. These effects were most probably mediated via its antiangiogenic effects because TSP-1 did not affect the growth of cultured murine vibrissae in the absence of a functional vascular system. These results identify a critical role of TSP-1 in the induction of anagen follicle involution, with potential implications for the therapeutic modulation of hair follicle growth.
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[h=1]Control of hair growth and follicle size by VEGF-mediated angiogenesis.[/h]
Yano K,
Brown LF,
Detmar M.
[h=3]Source[/h]Cutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital, Building 149, 13th Street, Charlestown, MA 02129, USA.
[h=3]Abstract[/h]The murine hair follicle undergoes pronounced cyclic expansion and regression, leading to rapidly changing demands for its vascular support. Our study aimed to quantify the cyclic changes of perifollicular vascularization and to characterize the biological role of VEGF for hair growth, angiogenesis, and follicle cycling. We found a significant increase in perifollicular vascularization during the growth phase (anagen) of the hair cycle, followed by regression of angiogenic blood vessels during the involution (catagen) and the resting (telogen) phase. Perifollicular angiogenesis was temporally and spatially correlated with upregulation of VEGF mRNA expression by follicular keratinocytes of the outer root sheath, but not by dermal papilla cells. Transgenic overexpression of VEGF in outer root sheath keratinocytes of hair follicles strongly induced perifollicular vascularization, resulting in accelerated hair regrowth after depilation and in increased size of hair follicles and hair shafts. Conversely, systemic treatment with a neutralizing anti-VEGF antibody led to hair growth retardation and reduced hair follicle size. No effects of VEGF treatment or VEGF blockade were observed in mouse vibrissa organ cultures, which lack a functional vascular system. These results identify VEGF as a major mediator of hair follicle growth and cycling and provide the first direct evidence that improved follicle vascularization promotes hair growth and increases hair follicle and hair size.
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[h=1]Active hair growth (anagen) is associated with angiogenesis.[/h]
Mecklenburg L,
Tobin DJ,
Müller-Röver S,
Handjiski B,
Wendt G,
Peters EM,
Pohl S,
Moll I,
Paus R.
[h=3]Source[/h]Department of Dermatology, University Hospital Eppendorf, University of Hamburg, Germany.
[h=3]Abstract[/h]After the completion of skin development, angiogenesis, i.e., the growth of new capillaries from pre-existing blood vessels, is held to occur in the skin only under pathologic conditions. It has long been noted, however, that hair follicle cycling is associated with prominent changes in skin perfusion, that the epithelial hair bulbs of anagen follicles display angiogenic properties, and that the follicular dermal papilla can produce angiogenic factors. Despite these suggestive observations, no formal proof is as yet available for the concept that angiogenesis is a physiologic event that occurs all over the mature mammalian integument whenever hair follicles switch from resting (telogen) to active growth (anagen). This study uses quantitative histomorphometry and double-immunohistologic detection techniques for the demarcation of proliferating endothelial cells, to show that synchronized hair follicle cycling in adolescent C57BL/6 mice is associated with substantial angiogenesis, and that inhibiting angiogenesis in vivo by the intraperitoneal application of a fumagillin derivative retards experimentally induced anagen development in these mice. Thus, angiogenesis is a physiologic event in normal postnatal murine skin, apparently is dictated by the hair follicle, and appears to be required for normal anagen development. Anagen-associated angiogenesis offers an attractive model for identifying the physiologic controls of cutaneous angiogenesis, and an interesting system for screening the effects of potential antiangiogenic drugs in vivo.
