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Bone Regeneration Effect of Cassia occidentalis Linn. Extract and Its Isolated Compounds
Published in Brijesh Kumar, Vikas Bajpai, Vikaskumar Gond, Subhashis Pal, Naibedya Chattopadhyay, Phytochemistry of Plants of Genus Cassia, 2021
Brijesh Kumar, Vikas Bajpai, Vikaskumar Gond, Subhashis Pal, Naibedya Chattopadhyay
NFκB is the major inflammatory molecule that not only supports osteoclastogenesis and bone resorption but also causes joint destruction in RA and OA. In a mouse model of collagen-induced RA, the so-called CIA model, emodin (10 mg/kg, i.p.) in a therapeutic mode (administered 25 days after collagen-II challenge) decreased the arthritis disease score, suppressed synovial inflammation and joint destruction. In the joints of CIA mice, the enhancement of NFκB signaling revealed by decreased cytoplasmic levels of inhibitor κB (IκB) and increased nuclear levels of p65 and p50 in the nuclear fraction was reversed by emodin treatment. Consequently, the CIA-induced elevations in inflammatory cytokines including TNFα, IL1β, RANKL and IL17 in the joints were decreased by emodin, as well as the serum levels of TNFα and IL1β. Furthermore, the matrix-degrading matrix metalloproteinases-1,3 (MMP1 and MMP3) levels that were increased in the joints of CIA mice were significantly suppressed by emodin treatment (Hwang, 2013).
Dermal Fibroblast Function
Published in Brian J. Nickoloff, Dermal Immune System, 2019
Enzymes synthesized by fibroblasts and other cells are capable of extensive degradation of all matrix components. The matrix metalloproteinases (MMPs) are interstitial collagenase (MMP-1), type IV collagenase (gelatinases, MMP-2), and stromelysins (MMP-3).55 The MMPs are likely the major rate-limiting enzymes controlling extracellular matrix degradation in normal and pathological conditions.55
Micronutrients in Prevention and Improvement of the Standard Therapy in Arthritis
Published in Kedar N. Prasad, Micronutrients in Health and Disease, 2019
Treatment of RA synovial fibroblasts in culture with epigallocatechin-3-gallate suppressed TNF-alpha-induced production of matrix metalloproteinase-1 (MMP-1) and MMP-3 that play a significant role in destruction of cartilage and bone in RA joint.72
Chymotrypsin attenuates adjuvant-induced arthritis by downregulating TLR4, NF-κB, MMP-1, TNF-α, IL-1β, and IL-6 expression in Sprague–Dawley rats
Published in Immunopharmacology and Immunotoxicology, 2022
Jianqiang Li, Linlin Wang, Guangting Zeng, Huilan Li, Jia Luo, Qijun Tian, Zanling Zhang
MMP-1 is a fibroblast collagenase that is primarily major implicated in mediating the degradation of type I, type II, and III collagens [22]. MMP-1 is expressed in RA, but was found to be expressed at a lower level in normal joint tissue [23]. Inflammatory factors such as IL-1 and TNF-α regulate the expression of the MMP gene by activating NF-κB regulated signal transduction pathways [24]. NF-κB plays an important role in controlling the expression of MMP in arthritis [25]. NF-kB is a dimer of the p50 and p65 subunits and is inactive in the cytoplasm when bound to the inhibitor of NF-kB (IkB). IkB tends to be phosphorylated and damaged when cells are stimulated with IL-1 or TNF-α. The p50 and RelA subunits dissociate from IkB and transfer to the nucleus, combine the binding sites in gene promoters and activate transcription [26]. The promoters of MMP-1 contain typical binding sites for NF-kB, and activation of NF-kB is important for upregulating MMP-1 expression [12].
Role of the BMP6 protein in breast cancer and other types of cancer
Published in Growth Factors, 2021
Andrea Marlene García Muro, Azaria García Ruvalcaba, Lourdes del Carmen Rizo de la Torre, Josefina Yoaly Sánchez López
Evidence in vitro studies indicate that BMP6 promotes cellular adherence, decreases migration and significantly inhibits the promoter activity of matrix metalloproteinase-1 (MMP-1) gene in a way dependent on the AP-1 site, MMP is considered an important factor in the invasion and metastasis processes of BC cells, on the other hand, the decrease in BMP6 is related to an epithelial-mesenchymal transition (EMT) phenotype, as well as BMP6 silencing in BC cells significantly increased cell growth and proliferation and caused a decrease in the cytotoxic effect of doxorubicin; the authors propose that DNA methylation can regulate the expression of BMP6 and that in turn, this regulates the EMT phenotype related to drug resistance in BC (Liu et al. 2014; Lian et al. 2013; de Boeck et al. 2016; Hu et al. 2016).
Expression of pulmonary arterial elastin in rats with hypoxic pulmonary hypertension using H2S
Published in Journal of Receptors and Signal Transduction, 2020
Juan Chen, Haizhou Zhang, Wancheng Yu, Lei Chen, Zhengjun Wang, Tao Zhang
Matrix protease-1 (MMP-1), as a collagenase, is mainly used for the degradation of type I, II and III collagens. TIMP-1 is a specific inhibitor of MMP-1. Through inhibiting the activation process of MMP zymogen, TIMPs reduce the activity of the activated MMPs and better inhibit collagen degradation. In this experiment, under the low oxygen conditions, the expression of middle-and-small pulmonary artery TIMP-1 mRNA expression of rats has up-regulated. This indicates that the increase of synthesis of TIMP-1 mRNA results in the decrease of degradation of collagen in pulmonary artery wall by MMP-1. As a result, the collagen in small and medium pulmonary arteries in hypoxic rats gradually accumulates. After adding H2S intervention, the expression of TIMP-1 mRNA in small and medium-sized pulmonary arteries was gradually down-regulated. This clearly shows that the reduction of TIMP-1 synthesis [20–23] is able to weaken the inhibition of MMP-1 expression and to gradually increase the degradation of pulmonary collagen. Fundamentally, the accumulation of medium-and-small pulmonary collagen of hypoxic rats gradually slows down [22,24–26]. This means that H2S can reduce TIMP-1 synthesis to degrade collagen, and further alleviating collagen accumulation in hypoxic rat pulmonary arteries [27–29].