BACKGROUND: Systemic sclerosis (SSc) is a connective tissue disorder characterized by tissue hypoxia and excessive fibrosis of skin and internal organs. OBJECTIVE: To evaluate the possible role of angiogenesis imbalance in the pathogenesis of SSc. SUBJECTS AND METHODS: Twenty-five SSc patients and 20 age- and sex-matched healthy controls were included. Assay of serum vascular endothelial growth factor (VEGF) and endostatin was done for all patients and controls using enzyme-linked immunosorbent assay. Patients were subjected to modified Rodnan skin score (mRss), pulmonary function tests (PFTS) and skin biopsies for histopathological skin thickness score assessment. RESULTS: There was significant increase in the mean levels of serum VEGF and endostatin in SSc patients compared to controls (t = 4.07, P < 0.001). Mean values of serum endostatin was significantly increased in late compared to early stages of disease (t = 6.65, P < 0.01). A significant positive correlation was found between serum levels of endostatin, mRss and histopathological skin thickness score (r = 0.99, 0.94, respectively, P < 0.01). SSc patients with ischemic manifestations had significantly higher levels of serum endostatin compared to those without ischemic manifestations (t = 6.27, P < 0.001). SSc patients with restricted PFTS had significantly higher levels of serum endostatin compared to those without pulmonary manifestations (t = 4.3, P < 0.001). CONCLUSION: Angiogenic inhibitor (endostatin) is induced and outweighs angiogenic inducer (VEGF) in late stages of SSc. Increased serum endostatin is associated with skin sclerosis severity and pulmonary fibrosis and favors SSc disease progression.
BACKGROUND:Systemic sclerosis (SSc) is a connective tissue disorder characterized by tissue hypoxia and excessive fibrosis of skin and internal organs. OBJECTIVE: To evaluate the possible role of angiogenesis imbalance in the pathogenesis of SSc. SUBJECTS AND METHODS: Twenty-five SSc patients and 20 age- and sex-matched healthy controls were included. Assay of serum vascular endothelial growth factor (VEGF) and endostatin was done for all patients and controls using enzyme-linked immunosorbent assay. Patients were subjected to modified Rodnan skin score (mRss), pulmonary function tests (PFTS) and skin biopsies for histopathological skin thickness score assessment. RESULTS: There was significant increase in the mean levels of serum VEGF and endostatin in SSc patients compared to controls (t = 4.07, P < 0.001). Mean values of serum endostatin was significantly increased in late compared to early stages of disease (t = 6.65, P < 0.01). A significant positive correlation was found between serum levels of endostatin, mRss and histopathological skin thickness score (r = 0.99, 0.94, respectively, P < 0.01). SSc patients with ischemic manifestations had significantly higher levels of serum endostatin compared to those without ischemic manifestations (t = 6.27, P < 0.001). SSc patients with restricted PFTS had significantly higher levels of serum endostatin compared to those without pulmonary manifestations (t = 4.3, P < 0.001). CONCLUSION: Angiogenic inhibitor (endostatin) is induced and outweighs angiogenic inducer (VEGF) in late stages of SSc. Increased serum endostatin is associated with skin sclerosis severity and pulmonary fibrosis and favors SSc disease progression.
Authors: Christopher A Mecoli; Jamie Perin; Jennifer E Van Eyk; Jie Zhu; Qin Fu; Andrew G Allmon; Youlan Rao; Scott Zeger; Fredrick M Wigley; Laura K Hummers; Ami A Shah Journal: Clin Rheumatol Date: 2019-12-19 Impact factor: 2.980
Authors: Chiara Bellocchi; Jun Ying; Ellen A Goldmuntz; Lynette Keyes-Elstein; John Varga; Monique E Hinchcliff; Marka A Lyons; Peter McSweeney; Daniel E Furst; Richard Nash; Leslie J Crofford; Beverly Welch; Jonathan G Goldin; Ashley Pinckney; Maureen D Mayes; Keith M Sullivan; Shervin Assassi Journal: Arthritis Rheumatol Date: 2021-02-28 Impact factor: 10.995