Institut National de la Santé et de la Recherche Médicale (INSERM, U1036), Grenoble F-38000, France; Commissariat à l'Énergie Atomique et aux Energies Alternatives, Institut de Recherches en Technologies et Sciences pour le Vivant, Laboratoire Biologie du Cancer et de l'Infection, Grenoble F-38000, France; Université Grenoble-Alpes, Grenoble F-38000, France. Electronic address:
Published: February 2016
AI Article Synopsis
Article Abstract
The vascular system is critical for developmental growth, tissue homeostasis and repair but also for tumor development. Bone morphogenetic protein (BMP) signaling has recently emerged as a fundamental pathway of the endothelium by regulating cardiovascular and lymphatic development and by being causative for several vascular dysfunctions. Two vascular disorders have been directly linked to impaired BMP signaling: pulmonary arterial hypertension and hereditary hemorrhagic telangiectasia. Endothelial BMP signaling critically depends on the cellular context, which includes among others vascular heterogeneity, exposure to flow, and the intertwining with other signaling cascades (Notch, WNT, Hippo and hypoxia). The purpose of this review is to highlight the most recent findings illustrating the clear need for reconsidering the role of BMPs in vascular biology.
Objective: Spinal cord injury (SCI) is a severe and permanent nerve damage condition that poses significant burdens on individuals and society. Various therapeutic approaches have been explored to mitigate the consequences of SCI. Tissue engineering and regenerative medicine have emerged as a promising avenue for addressing this issue.
Pulmonary hypertension (PH) encompasses a group of conditions which ultimately lead to elevated pulmonary arterial pressure. PH is classified into five subgroups, of which Group 1 pulmonary arterial hypertension (PAH), is the most extensively studied. Numerous causal genes have been identified in PAH, most notably germline mutations in bone morphogenetic protein receptor type 2 () and the wider BMP pathway.
Excessive mechanical overloading of articular cartilage caused by excessive exercise or severe trauma is considered a critical trigger in the development of osteoarthritis (OA). However, the available clinical theranostic molecular targets and underlying mechanisms still require more elucidation. Here, we aimed to examine the possibility that bone morphogenetic proteins (BMPs) serve as molecular targets in rat cartilages and human chondrocytes under conditions of excessive mechanical overloading.
Division of Anatomical and Cellular Pathology, Department of Pathology, Iwate Medical University, 1-1-1 Idaidori, Yahaba-cho, Shiwa-gun, Iwate, 028-3694, Japan. Electronic address:
Objective: This study aimed to evaluate the role of the chromodomain helicase DNA-binding protein 3 (CHD3) in tooth morphogenesis in Chd3 knockout mice.
Methods: Chd3 knockout mice were generated using the CRISPR-Cas9 method. Mandibular first molars were extracted from the mice and their littermates and morphometrically analyzed.
Background: Osteoporosis is a systemic skeletal disorder characterized by decreased bone mass and impaired bone microarchitecture because of an imbalance between bone resorption and formation. Existing pharmacological treatments often have significant side effects and mainly focus on inhibiting bone resorption. Other than inhibiting osteoclast-mediated bone resorption, the present study also investigates the potential role of sheepskin collagen peptide (SSCP) in bone formation by promoting osteoblast proliferation, differentiation and mineralization.
