Maackia amurensis seed lectin (MASL) ameliorates articular cartilage destruction and increases movement velocity of mice with TNFα induced rheumatoid arthritis.
Maackia amurensis seed lectin (MASL) ameliorates articular cartilage destruction and increases movement velocity of mice with TNFα induced rheumatoid arthritis.
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DOI：
10.1016/j.bbrep.2022.101341
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发表时间：
2022-12
影响因子：
2.7
通讯作者：
Goldberg, Gary S.
中科院分区：
文献类型：
--
作者：
Hamilton, Kelly L.;Greenspan, Amanda A.;Shienbaum, Alan J.;Fischer, Bradford D.;Bottaro, Andrea;Goldberg, Gary S.
全世界有多达7000万人患有类风湿性关节炎。目前的治疗方案具有不同的疗效，并可能导致不必要的副作用。需要新的方法来治疗这种情况。软骨细胞受体上的唾液酸修饰与关节炎炎症和关节破坏有关。例如，跨膜粘蛋白受体蛋白podoplanin（PDPN）已被鉴定为呈现细胞外唾液酸基序的功能相关受体。PDPN信号传导促进与关节炎相关的炎症和侵袭，因此已成为可用于抑制关节炎炎症的靶点。在脂多糖诱导的骨关节炎小鼠模型中，怀槐种子凝集素（MASL）可以靶向软骨细胞上的PDPN，以减少炎症信号级联并减少软骨破坏。在这里，我们研究了MASL对TNFα转基因（TNF-Tg）小鼠模型中类风湿性关节炎进展的影响。本研究的结果表明，MASL可以口服给药，以改善关节畸形和增加这些TNF-Tg小鼠表现出的运动速度。这些数据支持将MASL视为类风湿性关节炎的潜在治疗方法。TNF-Tg小鼠出现类风湿性关节炎症状和形态学。MASL给药降低TNF诱导的关节炎形态。MASL给药增加TNF-Tg小鼠的运动速度。MASL给药不会破坏小鼠体重、行为或组织形态。MASL给药减少TNF诱导的踝关节软骨破坏。
Up to 70 million people around the world suffer from rheumatoid arthritis. Current treatment options have varied efficacy and can cause unwanted side effects. New approaches are needed to treat this condition. Sialic acid modifications on chondrocyte receptors have been associated with arthritic inflammation and joint destruction. For example, the transmembrane mucin receptor protein podoplanin (PDPN) has been identified as a functionally relevant receptor that presents extracellular sialic acid motifs. PDPN signaling promotes inflammation and invasion associated with arthritis and, therefore, has emerged as a target that can be used to inhibit arthritic inflammation. Maackia amurensis seed lectin (MASL) can target PDPN on chondrocytes to decrease inflammatory signaling cascades and reduce cartilage destruction in a lipopolysaccharide induced osteoarthritis mouse model. Here, we investigated the effects of MASL on rheumatoid arthritis progression in a TNFα transgenic (TNF-Tg) mouse model. Results from this study indicate that MASL can be administered orally to ameliorate joint malformation and increase velocity of movement exhibited by these TNF-Tg mice. These data support the consideration of MASL as a potential treatment for rheumatoid arthritis. TNF-Tg mice develop rheumatoid arthritis symptoms and morphology. MASL administration decreases TNF induced arthritic morphology. MASL administration increases TNF-Tg mice movement velocity. MASL administration does not disrupt mouse weight, behavior, or tissue morphology. MASL administration decreases TNF induced ankle cartilage destruction.
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DOI：
10.1007/s00281-003-0125-3
发表时间：
2003-08-01
期刊：
SPRINGER SEMINARS IN IMMUNOPATHOLOGY
影响因子：
--
作者：
Li, P;Schwarz, EM
通讯作者：
Schwarz, EM
影响因子：
5.2
作者：
Clark MC;Baum LG
通讯作者：
Baum LG
影响因子：
11.4
作者：
KEFFER, J;PROBERT, L;KOLLIAS, G
通讯作者：
KOLLIAS, G
影响因子：
2.6
作者：
Batterman, Alexander, I;DeChiara, James;Ferraro, Thomas N.
通讯作者：
Ferraro, Thomas N.
影响因子：
--
作者：
Ochoa-Alvarez JA;Krishnan H;Pastorino JG;Nevel E;Kephart D;Lee JJ;Retzbach EP;Shen Y;Fatahzadeh M;Baredes S;Kalyoussef E;Honma M;Adelson ME;Kaneko MK;Kato Y;Young MA;Deluca-Rapone L;Shienbaum AJ;Yin K;Jensen LD;Goldberg GS
通讯作者：
Goldberg GS