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Biomaterials, Tissue Engineering and Their Application in the Oral and Maxillofacial Region
Published in John C Watkinson, Raymond W Clarke, Louise Jayne Clark, Adam J Donne, R James A England, Hisham M Mehanna, Gerald William McGarry, Sean Carrie, Basic Sciences Endocrine Surgery Rhinology, 2018
Kurt Busuttil Naudi, Ashraf Ayoub
A large mandibular discontinuity defect was repaired with a custom bone transplant grown inside the latissimus dorsi muscle of an adult male patient. This was achieved using computed tomography scanning and computer-aided design techniques to produce a virtual replacement (in the form of a titanium mesh) for the mandibular defect. This was filled with bone mineral blocks, recombinant human bone morphogenetic protein 7 and the patient’s bone marrow. Seven weeks after placement in the latissimus dorsi muscle the graft was successfully transplanted as a free bone-muscle flap to repair the mandibular defect.22
Differentiation of rat bone marrow mesenchymal stem cells into neurons induced by bone morphogenetic protein 7 in vitro
Published in Neurological Research, 2023
Heng Zhang, Lei Gao, Wen Zhang, Kuanxin Li
Bone morphogenetic protein 7 (BMP-7) is a member of the β transforming growth factor (TGF-β) superfamily. It has been reported that BMP-7 is closely related to the repair of the nervous system [8]. Kusakawa et al. found that BMP-7 was observed in astrocytes, gray matter nerve fibers, dopaminergic neurons, and noradrenergic neurons in the central nervous system by immunohistochemistry [9]. Setoguchi et al. also indicate that BMP-7 plays an important role in the development of the central nervous system [10]. In the infarct model of middle cerebral artery occlusion treated by BMP-7 transplantation, the infarct size of mice is decreased, indicating that BMP-7 has neuroprotective effect [11]. BMP-7 mRNA level is decreased in the uninjured spinal cord, but increased in the spinal cord tissue after SCI. It is speculated that BMP-7 plays a protective role in the early stage of spinal cord injury [12].
Zaprinast and avanafil increase the vascular endothelial growth factor, vitamin D3, bone morphogenic proteins 4 and 7 levels in the kidney tissue of male rats applied the glucocorticoid
Published in Archives of Physiology and Biochemistry, 2022
Zübeyir Huyut, Nuri Bakan, Halil İbrahim Akbay, Serkan Yıldırım, Mehmet Ramazan Şekeroğlu
BMP7 that we measure in the renal tissue plays an important role in the development of different tissues such as bone, kidney and brown adipose tissue (Xu et al. 2018). BMP7 not only has great potential in bone repair applications, but it also exhibit features as an cartilage banabolic factor due to its ability to induce matrix synthesis and promote cartilage repair (Deng et al. 2018). Normally produced and secreted by the kidney, bone morphogenetic protein 7 (BMP-7) maintains renal homeostasis and epithelial cell phenotype. BMP7 administration in different models of acute and chronic renal disease has been reported to be important in the preservation of renal tissue because it can preserve the phenotype of tubular epithelial cells, induce tissue regeneration, and reduce inflammatory response and cell apoptosis (Celic et al. 2018).
Renal fibrosis as a hallmark of diabetic kidney disease: potential role of targeting transforming growth factor-beta (TGF-β) and related molecules
Published in Expert Opinion on Therapeutic Targets, 2022
Jiali Tang, Fang Liu, Mark E. Cooper, Zhonglin Chai
In addition to regulating the transcription of fibrotic genes by the TGF-β/Smad signaling pathway, the TGF-β pathway interacts with a number of other signaling pathways [14,53]. There are some molecules that are not intrinsic components of the TGF-β pathway yet are able to modulate TGF-β signal transduction. Previous studies have demonstrated that bone morphogenetic protein 7 (BMP7) and hepatocyte growth factor (HGF) were able to antagonize TGF-β signaling. In contrast, cell division autoantigen 1 (CDA1) was found to enhance TGF-β signaling in DKD [188]. Thus, it is postulated that targeting these molecules should reduce the strength of TGF-β signaling yet avoid the risk of total blockade of the TGF-β pathway, leading to a safe and efficacious approach to combat renal fibrosis in DKD (Figure 5).