Bone Morphogenetic Proteins and Signaling Pathway in Inflammatory Bowel Disease

Marić, Ivana; Wensveen, Tamara Turk; Smoljan, Ivana; Orlić, Željka Crnčević; Bobinac, Dragica

doi:10.5772/29427

Cited by 4 publications

(6 citation statements)

References 133 publications

(118 reference statements)

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“…Deleting BMPR1a in CD4 + T cells impairs generation of iT reg cells and promotes pro-inflammatory function of TGF-b by supporting differentiation of Th17 cells (Browning et al, 2018;Kuczma et al, 2014). These data are consistent with reports demonstrating that inhibition of the BMP signaling in rheumatoid arthritis patients augmented inflammation induced by IL-17 and that BMPs ameliorated intestinal and renal inflammation (Maric et al, 2012;Takabayashi et al, 2014;Varas et al, 2015;Zeisberg et al, 2003). Our report reveals that BMPR1a is not only an important regulator of embryonic development and stem/progenitor cell-fate decisions but also controls immune homeostasis and inflammation (Bragdon et al, 2011;Miyazono et al, 2010).…”

Section: Discussionsupporting

confidence: 86%

Bone Morphogenic Proteins Are Immunoregulatory Cytokines Controlling FOXP3+ Treg Cells

et al. 2020

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Section: Discussionsupporting

confidence: 86%

Bone Morphogenic Proteins Are Immunoregulatory Cytokines Controlling FOXP3+ Treg Cells

et al. 2020

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“…In contrast, blockade of BMP signaling in rheumatoid arthritis patients with specific inhibitors augments inflammation induced by IL-17 (77). Consistent with our results, BMPs ameliorate intestinal inflammation and protect from mucosal damage (78,79). This role of BMPs on July 11, 2020 http://stke.sciencemag.org/ Downloaded from contrasts with recent reports that dorsomorphin and DMH1 (dorsomorphin homolog 1), which are small-molecule inhibitors of BMP receptors and other kinases, impede proliferation of human and mouse T cells and block T H 17 differentiation (27,80,81).…”

Section: Increased T H 1 Differentiation Of Bmpr1-deficient Cells Resupporting

confidence: 85%

TGF-β–mediated enhancement of T _H 17 cell generation is inhibited by bone morphogenetic protein receptor 1α signaling

et al. 2018

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The cytokines of the transforming growth factor-β (TGF-β) family promote the growth and differentiation of multiple tissues, but the role of only the founding member, TGF-β, in regulating the immune responses has been extensively studied. TGF-β is critical to prevent the spontaneous activation of self-reactive T cells and sustain immune homeostasis. In contrast, in the presence of proinflammatory cytokines, TGF-β promotes the differentiation of effector T helper 17 (T17) cells. Abrogating TGF-β receptor signaling prevents the development of interleukin-17 (IL-17)-secreting cells and protects mice from T17 cell-mediated autoimmunity. We found that the receptor of another member of TGF-β family, bone morphogenetic protein receptor 1α (BMPR1α), regulates T helper cell activation. We found that the differentiation of T17 cells from naive CD4 T cells was inhibited in the presence of BMPs. Abrogation of BMPR1α signaling during CD4 T cell activation induced a developmental program that led to the generation of inflammatory effector cells expressing large amounts of IL-17, IFN-γ, and TNF family cytokines and transcription factors defining the T17 cell lineage. We found that TGF-β and BMPs cooperated to establish effector cell functions and the cytokine profile of activated CD4 T cells. Together, our data provide insight into the immunoregulatory function of BMPs.

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“…In our study, the expression of the BMP2 gene was upregulated, which was consistent with a study conducted in a murine colitis model where TNBS was used as an inducer [ 11 ]. Furthermore, higher BMP2 expression in TNBS-induced colonic inflammation might be coupled with decreased sensitivity or lack of inhibitory factors [ 6 , 38 ] leading to enhanced epithelial cell proliferation [ 7 ]. In addition, the upregulation of BMP7b expression activates the MMP13 gene [ 39 ] for extracellular cell degradation in cartilage and bone joints, which causes cartilage degeneration [ 40 ].…”

Section: Discussionmentioning

confidence: 99%

“…They play a pivotal role [ 3 ] during the onset of inflammatory diseases [ 4 ]. As a result, several inflammatory disorders, including gut inflammation and arthritis, have pathological features connected to changes in BMP expression and the BMP signalling pathway [ 5 , 6 ].…”

Section: Introductionmentioning

confidence: 99%

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In Silico Study and Effects of BDMC33 on TNBS-Induced BMP Gene Expressions in Zebrafish Gut Inflammation-Associated Arthritis

et al. 2022

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The bone morphogenic protein (BMP) family is a member of the TGF-beta superfamily and plays a crucial role during the onset of gut inflammation and arthritis diseases. Recent studies have reported a connection with the gut–joint axis; however, the genetic players are still less explored. Meanwhile, BDMC33 is a newly synthesized anti-inflammatory drug candidate. Therefore, in our present study, we analysed the genome-wide features of the BMP family as well as the role of BMP members in gut-associated arthritis in an inflammatory state and the ability of BDMC33 to attenuate this inflammation. Firstly, genome-wide analyses were performed on the BMP family in the zebrafish genome, employing several in silico techniques. Afterwards, the effects of curcumin analogues on BMP gene expression in zebrafish larvae induced with TNBS (0.78 mg/mL) were determined using real time-qPCR. A total of 38 identified BMP proteins were revealed to be clustered in five major clades and contain TGF beta and TGF beta pro peptide domains. Furthermore, BDMC33 suppressed the expression of four selected BMP genes in the TNBS-induced larvae, where the highest gene suppression was in the BMP2a gene (an eight-fold decrement), followed by BMP7b (four-fold decrement), BMP4 (four-fold decrement), and BMP6 (three-fold decrement). Therefore, this study reveals the role of BMPs in gut-associated arthritis and proves the ability of BDMC33 to act as a potential anti-inflammatory drug for suppressing TNBS-induced BMP genes in zebrafish larvae.

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Bone Morphogenetic Proteins and Signaling Pathway in Inflammatory Bowel Disease

Cited by 4 publications

References 133 publications

Bone Morphogenic Proteins Are Immunoregulatory Cytokines Controlling FOXP3+ Treg Cells

Bone Morphogenic Proteins Are Immunoregulatory Cytokines Controlling FOXP3+ Treg Cells

TGF-β–mediated enhancement of T _H 17 cell generation is inhibited by bone morphogenetic protein receptor 1α signaling

In Silico Study and Effects of BDMC33 on TNBS-Induced BMP Gene Expressions in Zebrafish Gut Inflammation-Associated Arthritis

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Bone Morphogenetic Proteins and Signaling Pathway in Inflammatory Bowel Disease

Cited by 4 publications

References 133 publications

Bone Morphogenic Proteins Are Immunoregulatory Cytokines Controlling FOXP3+ Treg Cells

Bone Morphogenic Proteins Are Immunoregulatory Cytokines Controlling FOXP3+ Treg Cells

TGF-β–mediated enhancement of T H 17 cell generation is inhibited by bone morphogenetic protein receptor 1α signaling

In Silico Study and Effects of BDMC33 on TNBS-Induced BMP Gene Expressions in Zebrafish Gut Inflammation-Associated Arthritis

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TGF-β–mediated enhancement of T _H 17 cell generation is inhibited by bone morphogenetic protein receptor 1α signaling