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- W2016455961 abstract "Background Scleroderma is an autoimmune disease with a characteristic vascular pathology. The vasculopathy associated with scleroderma is one of the major contributors to the clinical manifestations of the disease. Methodology/Principal Findings We used immunohistochemical and mRNA in situ hybridization techniques to characterize this vasculopathy and showed with morphometry that scleroderma has true capillary rarefaction. We compared skin biopsies from 23 scleroderma patients and 24 normal controls and 7 scleroderma patients who had undergone high dose immunosuppressive therapy followed by autologous hematopoietic cell transplant. Along with the loss of capillaries there was a dramatic change in endothelial phenotype in the residual vessels. The molecules defining this phenotype are: vascular endothelial cadherin, a supposedly universal endothelial marker required for tube formation (lost in the scleroderma tissue), antiangiogenic interferon α (overexpressed in the scleroderma dermis) and RGS5, a signaling molecule whose expression coincides with the end of branching morphogenesis during development and tumor angiogenesis (also overexpressed in scleroderma skin. Following high dose immunosuppressive therapy, patients experienced clinical improvement and 5 of the 7 patients with scleroderma had increased capillary counts. It was also observed in the same 5 patients, that the interferon α and vascular endothelial cadherin had returned to normal as other clinical signs in the skin regressed, and in all 7 patients, RGS5 had returned to normal. Conclusion/Significance These data provide the first objective evidence for loss of vessels in scleroderma and show that this phenomenon is reversible. Coordinate changes in expression of three molecules already implicated in angiogenesis or anti-angiogenesis suggest that control of expression of these three molecules may be the underlying mechanism for at least the vascular component of this disease. Since rarefaction has been little studied, these data may have implications for other diseases characterized by loss of capillaries including hypertension, congestive heart failure and scar formation." @default.
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- W2016455961 date "2008-01-16" @default.
- W2016455961 modified "2023-10-02" @default.
- W2016455961 title "Capillary Regeneration in Scleroderma: Stem Cell Therapy Reverses Phenotype?" @default.
- W2016455961 cites W1497601632 @default.
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- W2016455961 cites W1545946482 @default.
- W2016455961 cites W1876338319 @default.
- W2016455961 cites W1879008659 @default.
- W2016455961 cites W1923133386 @default.
- W2016455961 cites W1942070062 @default.
- W2016455961 cites W1975965422 @default.
- W2016455961 cites W1978171344 @default.
- W2016455961 cites W1980755389 @default.
- W2016455961 cites W1984043167 @default.
- W2016455961 cites W1986513431 @default.
- W2016455961 cites W1988379927 @default.
- W2016455961 cites W1988719246 @default.
- W2016455961 cites W1990552167 @default.
- W2016455961 cites W1997773937 @default.
- W2016455961 cites W2000597449 @default.
- W2016455961 cites W2001929118 @default.
- W2016455961 cites W2003225450 @default.
- W2016455961 cites W2003859885 @default.
- W2016455961 cites W2006772331 @default.
- W2016455961 cites W2013295033 @default.
- W2016455961 cites W2016830520 @default.
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- W2016455961 cites W2035371785 @default.
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- W2016455961 cites W2054256551 @default.
- W2016455961 cites W2056690052 @default.
- W2016455961 cites W2063739726 @default.
- W2016455961 cites W2076931480 @default.
- W2016455961 cites W2084274322 @default.
- W2016455961 cites W2084308937 @default.
- W2016455961 cites W2093915058 @default.
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- W2016455961 cites W2125202148 @default.
- W2016455961 cites W2125701590 @default.
- W2016455961 cites W2125881724 @default.
- W2016455961 cites W2132698003 @default.
- W2016455961 cites W2139405922 @default.
- W2016455961 cites W2142932912 @default.
- W2016455961 cites W2143222045 @default.
- W2016455961 cites W2147639753 @default.
- W2016455961 cites W2152899507 @default.
- W2016455961 cites W2158509515 @default.
- W2016455961 cites W2159133324 @default.
- W2016455961 cites W2160641591 @default.
- W2016455961 cites W2169090892 @default.
- W2016455961 cites W2183175840 @default.
- W2016455961 cites W2194405934 @default.
- W2016455961 cites W2340723331 @default.
- W2016455961 cites W2408317903 @default.
- W2016455961 cites W2414574987 @default.
- W2016455961 cites W2463726114 @default.
- W2016455961 cites W282283539 @default.
- W2016455961 cites W32167704 @default.
- W2016455961 cites W4238556574 @default.
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- W2016455961 doi "https://doi.org/10.1371/journal.pone.0001452" @default.
- W2016455961 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2175530" @default.
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- W2016455961 hasPublicationYear "2008" @default.
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