Motivating role of type H vessels in bone regeneration

Abstract

Coupling between angiogenesis and osteogenesis has an important role in both normal bone injury repair and successful application of tissue‐engineered bone for bone defect repair. Type H blood vessels are specialized microvascular components that are closely related to the speed of bone healing. Interactions between type H endothelial cells and osteoblasts, and high expression of CD31 and EMCN render the environment surrounding these blood vessels rich in factors conducive to osteogenesis and promote the coupling of angiogenesis and osteogenesis. Type H vessels are mainly distributed in the metaphysis of bone and densely surrounded by Runx2+ and Osterix+ osteoprogenitors. Several other factors, including hypoxia‐inducible factor‐1α, Notch, platelet‐derived growth factor type BB, and slit guidance ligand 3 are involved in the coupling of type H vessel formation and osteogenesis. In this review, we summarize the identification and distribution of type H vessels and describe the mechanism for type H vessel‐mediated modulation of osteogenesis. Type H vessels provide new insights for detection of the molecular and cellular mechanisms that underlie the crosstalk between angiogenesis and osteogenesis. As a result, more feasible therapeutic approaches for treatment of bone defects by targeting type H vessels may be applied in the future.

Novel computational analysis of large transcriptome datasets identifies sets of genes distinguishing chronic obstructive pulmonary disease from healthy lung samples

“…Genes are sorted by the mRNA regulation in COPD and gene symbol (alphabetic). Name Gene symbol mRNA regulation in COPD Literature evidence supporting a role in COPD Autophagy related 3 ATG3 Up Positive regulator of autophagy, involved in TGF-β induced epithelial-to-mesenchymal transition in alveolar epithelial A549 cells 22 Chimerin 2 CHN2 Up Activator of RAC1 23 (see Table 3 ) Dihydropyrimidinase DPYS Up Upregulated in response to long-term (9 months) cigarette smoke exposure in mice 24 Growth arrest specific 2 GAS2 Up Shown to modulate cell cycle and apoptosis 25 in a non-COPD context Gametogenetin GGN Up – Cysteine rich protein 1 CRIP1 Down Indirect evidence: CRIP1 acts as carrier for transmucosal zinc absorption 26 . COPD is associated with pulmonary zinc deficiency and in vitro zinc depletion causes bronchial epithelial apoptosis and impairs apoptotic cell clearance 27 Dipeptidyl peptidase like 6 DPP6 Down Indirect evidence: DPP6 is a positive regulator of Kv4 potassium channels 28 .…”

Low level laser therapy promotes bone regeneration by coupling angiogenesis and osteogenesis

“…Crosstalk between MSCs and the vascular network is the basis of bone formation, remodeling, and healing processes, and the recruitment and migration of endothelial cells are critical to these processes [ 31 – 33 ]. Recent studies have confirmed that type H blood vessels and bone formation are closely related [ 34 ]. Low energy laser therapy has many biological effects.…”

“…Recent studies have identified the CD31 hi EMCN hi vascular endothelium that positively regulates bone formation, bone maturation, and regeneration. Studies have shown that type H vessel coupling bone formation is involved in a variety of factors, including HIF-1α, Notch, VEGF, platelet-derived growth factor type BB (PDGF-BB), slit guidance ligand 3 (SLIT3) [ 12 , 34 , 49 , 50 ]. Given that LLLT has the dual effect of promoting tube formation by ECs and the osteogenic differentiation of stem cells, and our results also confirmed that LLLT could further enhance tube formation and osteogenic differentiation in a co-culture cell system, we hypothesized that LLLT may exert those effects through coupling of angiogenesis to osteogenesis.…”

Cutting Edge Endogenous Promoting and Exogenous Driven Strategies for Bone Regeneration

“…In fact, the peptide 152RM (PTP1B Y152 region-mimicking peptide) loaded onto DMB scaffolds with mesoporous silica nanoparticles (MSNs) [ 78 ] significantly inhibited the phosphorylation of PTP1B Y152 [ 79 ], enhanced MSCs migration and osteogenic differentiation. Moreover, in vivo studies showed that this scaffold coupled the osteogenesis and angiogenesis processes, by inducing bone formation and the expansion of a certain type of blood vessels adjacent to the growth plate, closely related to the speed of bone healing [ 80 ].…”