We are analyzing https://link.springer.com/article/10.1007/s00296-003-0379-z.

Title:
Disease-associated increased HIF-1, αvβ3 integrin, and Flt-1 do not suffice to compensate the damage-inducing loss of blood vessels in inflammatory myopathies | Rheumatology International
Description:
Objective To analyze the microvascular network in skeletal muscle biopsies from patients with dermatomyositis (DM) and systemic sclerosis (SSc) compared to polymyositis (PM) and systemic lupus erythematosus (SLE), and non-inflammatory myopathies, and to clarify whether reparative angiogenesis-related factors are expressed in parallel to blood vessel damage. Methods Immunohistochemical staining of muscle biopsies (10 DM, 10 SSc, 10 PM, 10 SLE, and 10 non-inflammatory myopathies) with antibodies against von Willebrand factor (vWF), hypoxia-inducible factor-1β (HIF-1β), β3 integrin subunit, and vascular endothelial growth factor receptor-1 (VEGFR-1). The TechMate staining robot and biotin-streptavidin protocol were used. Results DM and SSc muscles were characterized by endothelial damage and reduction of blood vessel network. Expression of angiogenesis-related factors (HIF-1β, β3, VEGFR-1) was also found in the same biopsies. In contrast, in PM and SLE muscles, vascular networks were apparently not affected and angiogenic stimuli were less expressed if at all. Conclusions This work demonstrates that in inflamed muscles hypoxia/ischemia induces increased expression of angiogenic factors, yet their impact is insufficient to repair disease-associated reduction of the capillary network. This leads to questions considering the usefulness of angiogenic factors in the treatment of ischemic inflammatory myopathies in DM and SSc.
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Keywords {🔍}

google, scholar, cas, pubmed, article, muscle, factor, inflammatory, myopathies, vascular, endothelial, growth, dermatomyositis, systemic, helsinki, blood, konttinen, expression, rheumatol, med, cell, integrin, skeletal, capillary, access, angiogenesis, university, privacy, cookies, content, flt, yrjö, mackiewicz, microvascular, patients, sclerosis, polymyositis, factors, angiogenic, idiopathic, hypoxia, finland, publish, research, search, vessels, zygmunt, biopsies, ssc, damage,

Topics {✒️}

systemic lupus erythematosus month download article/chapter mediate hypoxia-initiated angiogenesis reparative angiogenesis-related factors idiopathic inflammatory myopathy hypoxia-inducible factor-1β idiopathic inflammatory myopathies angiogenesis-related transcription full article pdf placenta growth factor inflamed synovial membrane von willebrand factor privacy choices/manage cookies lymphocyte-induced angiogenesis angiogenesis-related factors hypoxia-inducible factor 1 enhanced pathological angiogenesis excercise-induced expression systemic sclerosis 2017 systemic sclerosis systemic sclerosis interleukin-1α expression cell surface marker ischemic inflammatory myopathies intramuscular blood vessels decreased capillary density sustaining autoimmune myositis myositis-specific autoantibodies skeletal muscle cells european economic area techmate staining robot biotin-streptavidin protocol cellular immune mechanisms flk-1 mrnr levels skillful technical assistance bioanalyst eija kaila muscle capillary damage conditions privacy policy blood vessel damage β3 integrin subunit pedro-botet jc exercise-induced vegf sigrid juselius foundation medicine/invärtes medicin blood vessel network damage-inducing loss human skeletal muscle related subjects ann neurol 37[s1] accepting optional cookies

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         headline:Disease-associated increased HIF-1, αvβ3 integrin, and Flt-1 do not suffice to compensate the damage-inducing loss of blood vessels in inflammatory myopathies
         description:To analyze the microvascular network in skeletal muscle biopsies from patients with dermatomyositis (DM) and systemic sclerosis (SSc) compared to polymyositis (PM) and systemic lupus erythematosus (SLE), and non-inflammatory myopathies, and to clarify whether reparative angiogenesis-related factors are expressed in parallel to blood vessel damage. Immunohistochemical staining of muscle biopsies (10 DM, 10 SSc, 10 PM, 10 SLE, and 10 non-inflammatory myopathies) with antibodies against von Willebrand factor (vWF), hypoxia-inducible factor-1β (HIF-1β), β3 integrin subunit, and vascular endothelial growth factor receptor-1 (VEGFR-1). The TechMate staining robot and biotin-streptavidin protocol were used. DM and SSc muscles were characterized by endothelial damage and reduction of blood vessel network. Expression of angiogenesis-related factors (HIF-1β, β3, VEGFR-1) was also found in the same biopsies. In contrast, in PM and SLE muscles, vascular networks were apparently not affected and angiogenic stimuli were less expressed if at all. This work demonstrates that in inflamed muscles hypoxia/ischemia induces increased expression of angiogenic factors, yet their impact is insufficient to repair disease-associated reduction of the capillary network. This leads to questions considering the usefulness of angiogenic factors in the treatment of ischemic inflammatory myopathies in DM and SSc.
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      description:To analyze the microvascular network in skeletal muscle biopsies from patients with dermatomyositis (DM) and systemic sclerosis (SSc) compared to polymyositis (PM) and systemic lupus erythematosus (SLE), and non-inflammatory myopathies, and to clarify whether reparative angiogenesis-related factors are expressed in parallel to blood vessel damage. Immunohistochemical staining of muscle biopsies (10 DM, 10 SSc, 10 PM, 10 SLE, and 10 non-inflammatory myopathies) with antibodies against von Willebrand factor (vWF), hypoxia-inducible factor-1β (HIF-1β), β3 integrin subunit, and vascular endothelial growth factor receptor-1 (VEGFR-1). The TechMate staining robot and biotin-streptavidin protocol were used. DM and SSc muscles were characterized by endothelial damage and reduction of blood vessel network. Expression of angiogenesis-related factors (HIF-1β, β3, VEGFR-1) was also found in the same biopsies. In contrast, in PM and SLE muscles, vascular networks were apparently not affected and angiogenic stimuli were less expressed if at all. This work demonstrates that in inflamed muscles hypoxia/ischemia induces increased expression of angiogenic factors, yet their impact is insufficient to repair disease-associated reduction of the capillary network. This leads to questions considering the usefulness of angiogenic factors in the treatment of ischemic inflammatory myopathies in DM and SSc.
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