Abnormal accumulation of collagen fibrils is a hallmark feature of oral submucous fibrosis(OSF).However,the precise characteristics and underlying mechanisms remain unclear,impeding the advancement of potential therap...Abnormal accumulation of collagen fibrils is a hallmark feature of oral submucous fibrosis(OSF).However,the precise characteristics and underlying mechanisms remain unclear,impeding the advancement of potential therapeutic approaches.Here,we observed that collagen Ⅰ,the main component of the extracellular matrix,first accumulated in the lamina propria and subsequently in the submucosa of OSF specimens as the disease progressed.Using RNA-seq and Immunofluorescence in OSF specimens,we screened the cartilage oligomeric matrix protein(COMP)responsible for the abnormal collagen accumulation.Genetic COMP deficiency reduced arecoline-stimulated collagen I deposition significantly in vivo.In comparison,both COMP and collagen Ⅰ were upregulated under arecoline stimulation in wild-type mice.Human oral buccal mucosal fibroblasts(hBMFs)also exhibited increased secretion of COMP and collagen I after stimulation in vitro.COMP knockdown in hBMFs downregulates arecoline-stimulated collagen Ⅰ secretion.We further demonstrated that hBMFs present heterogeneous responses to arecoline stimulation,of which COMP-positive fibroblasts secrete more collagen Ⅰ.Since COMP is a molecular bridge with Fibril-associated collagens with Interrupted Triple helices(FACIT)in the collagen network,we further screened and identified collagen XIV,a FACIT member,co-localizing with both COMP and collagen Ⅰ.Collagen XIV expression increased under arecoline stimulation in wild-type mice,whereas it was hardly expressed in the Comp^(-/-) mice,even with under stimulation.In summary,we found that COMP may mediates abnormal collagen Ⅰ deposition by functions with collagen XIV during the progression of OSF,suggesting its potential to be targeted in treating OSF.展开更多
大尺度植被光能利用率(light use efficiency,LUE)的快速准确获取一直是限制植被生产力估算及相关研究的难题。当前LUE的研究存在取值不准、方法复杂、精度不高等问题,而遥感数据时间连续、空间尺度大、易获取的优势为LUE的准确估算提...大尺度植被光能利用率(light use efficiency,LUE)的快速准确获取一直是限制植被生产力估算及相关研究的难题。当前LUE的研究存在取值不准、方法复杂、精度不高等问题,而遥感数据时间连续、空间尺度大、易获取的优势为LUE的准确估算提供了可能。以东北地区典型的芦苇湿地为研究对象,利用多时相遥感影像Landsat OLI(operational land imager)与植被指数,通过分析LUE、植被指数与植被叶绿素含量之间的关系,探讨利用遥感植被指数实现湿地植被LUE准确估算的可行性。结果表明:除增强植被指数(enhanced vegetation index,EVI)外,其余植被指数均有较强的芦苇湿地表征能力。LUE与叶绿素及植被指数之间存在密切关系,其中归一化植被指数(normalized difference vegetation index,NDVI)对LUE的敏感性最高(P <0.01;R^2=0.62),是本研究中表征芦苇LUE的最佳指数。研究验证了以叶绿素作为中间变量,借助遥感植被指数实现LUE便捷高效反演的理论假设,可为大尺度湿地植被生产力及碳循环等研究提供方法参考和思路借鉴。展开更多
基金supported by the National Natural Science Foundation of China grant(81974150).
文摘Abnormal accumulation of collagen fibrils is a hallmark feature of oral submucous fibrosis(OSF).However,the precise characteristics and underlying mechanisms remain unclear,impeding the advancement of potential therapeutic approaches.Here,we observed that collagen Ⅰ,the main component of the extracellular matrix,first accumulated in the lamina propria and subsequently in the submucosa of OSF specimens as the disease progressed.Using RNA-seq and Immunofluorescence in OSF specimens,we screened the cartilage oligomeric matrix protein(COMP)responsible for the abnormal collagen accumulation.Genetic COMP deficiency reduced arecoline-stimulated collagen I deposition significantly in vivo.In comparison,both COMP and collagen Ⅰ were upregulated under arecoline stimulation in wild-type mice.Human oral buccal mucosal fibroblasts(hBMFs)also exhibited increased secretion of COMP and collagen I after stimulation in vitro.COMP knockdown in hBMFs downregulates arecoline-stimulated collagen Ⅰ secretion.We further demonstrated that hBMFs present heterogeneous responses to arecoline stimulation,of which COMP-positive fibroblasts secrete more collagen Ⅰ.Since COMP is a molecular bridge with Fibril-associated collagens with Interrupted Triple helices(FACIT)in the collagen network,we further screened and identified collagen XIV,a FACIT member,co-localizing with both COMP and collagen Ⅰ.Collagen XIV expression increased under arecoline stimulation in wild-type mice,whereas it was hardly expressed in the Comp^(-/-) mice,even with under stimulation.In summary,we found that COMP may mediates abnormal collagen Ⅰ deposition by functions with collagen XIV during the progression of OSF,suggesting its potential to be targeted in treating OSF.
