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Article ; Online: 3D Biomimetic Calcified Cartilaginous Callus that Induces Type H Vessels Formation and Osteoclastogenesis

Minglong Qiu / Changwei Li / Zhengwei Cai / Cuidi Li / Kai Yang / Nijiati Tulufu / Bo Chen / Liang Cheng / Chengyu Zhuang / Zhihong Liu / Jin Qi / Wenguo Cui / Lianfu Deng

Advanced Science, Vol 10, Iss 16, Pp n/a-n/a (2023)

2023

Abstract: Abstract The formation of a calcified cartilaginous callus (CACC) is crucial during bone repair. CACC can stimulate the invasion of type H vessels into the callus to couple angiogenesis and osteogenesis, induce osteoclastogenesis to resorb the calcified ... ...

Abstract	Abstract The formation of a calcified cartilaginous callus (CACC) is crucial during bone repair. CACC can stimulate the invasion of type H vessels into the callus to couple angiogenesis and osteogenesis, induce osteoclastogenesis to resorb the calcified matrix, and promote osteoclast secretion of factors to enhance osteogenesis, ultimately achieving the replacement of cartilage with bone. In this study, a porous polycaprolactone/hydroxyapatite‐iminodiacetic acid‐deferoxamine (PCL/HA‐SF‐DFO) 3D biomimetic CACC is developed using 3D printing. The porous structure can mimic the pores formed by the matrix metalloproteinase degradation of the cartilaginous matrix, HA‐containing PCL can mimic the calcified cartilaginous matrix, and SF anchors DFO onto HA for the slow release of DFO. The in vitro results show that the scaffold significantly enhances angiogenesis, promotes osteoclastogenesis and resorption by osteoclasts, and enhances the osteogenic differentiation of bone marrow stromal stem cells by promoting collagen triple helix repeat‐containing 1 expression by osteoclasts. The in vivo results show that the scaffold significantly promotes type H vessels formation and the expression of coupling factors to promote osteogenesis, ultimately enhancing the regeneration of large‐segment bone defects in rats and preventing dislodging of the internal fixation screw. In conclusion, the scaffold inspired by biological bone repair processes effectively promotes bone regeneration.
Keywords	3D printing ; biomimetic calcified cartilaginous callus ; osteoclastogenesis ; osteogenesis ; type H vessels ; Science ; Q
Subject code	616
Language	English
Publishing date	2023-06-01T00:00:00Z
Publisher	Wiley
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Directed elimination of senescent cells attenuates development of osteoarthritis by inhibition of c-IAP and XIAP.

Peilin, Wang / Songsong, Teng / Chengyu, Zhuang / Zhi, Cui / Chunhui, Ma / Yinxian, Yu / Lei, Zhou / Min, Mao / Zongyi, Wang / Mengkai, Yang / Jing, Xu / Tao, Zhang / Zhuoying, Wang / Fei, Yin / Chengqing, Yi

Biochimica et biophysica acta. Molecular basis of disease

2019 Volume 1865, Issue 10, Page(s) 2618–2632

Abstract: Aging drives the accumulation of senescent cells (SnCs) by secreting factors that cause the senescence-associated secretory phenotype (SASP), including stem cells in the bone marrow, which contribute to aging-related bone degradation. Osteoarthritis (OA) ...

Abstract	Aging drives the accumulation of senescent cells (SnCs) by secreting factors that cause the senescence-associated secretory phenotype (SASP), including stem cells in the bone marrow, which contribute to aging-related bone degradation. Osteoarthritis (OA) is a serious chronic injury disease, and increasing age is a major risk factor. The accumulation of SnCs may accelerate the development of OA, and the accumulation of SnCs may benefit from its resistance to apoptotic stimuli. Therefore, local elimination of SnCs could be a promising treatment for OA. Apoptosis inhibitor protein (IAP) is an important antiapoptotic protein in vivo. AT-406 is a small molecule inhibitor of the IAP genes and also regulates the transcription of several genes. Here, we show that SnCs upregulate the antiapoptotic proteins c-IAP1, c-IAP2 and XIAP.The combined inhibition of c-IAP1, c-IAP2 and XIAP using siRNA or AT-406 specifically induce the apoptosis of SnCs.In addition, XIAP and STX17 bind to each other to regulate the fusion of autophagosomes and lysosomes in SnCs, which in turn, affects the fate of SnCs. It is worth noting that the clearance of SnCs attenuated the secretion of SASP and created a proregenerative environment. Most importantly, local clearance of SnCs significantly attenuated the progression of osteoarthritis in rats without significant toxic effects. Thus, local elimination of SnCs may be a potential treatment for OA. This is the first report of inhibition of IAPs for clearing SnCs and suggests that eradication of SnCs may be a new strategy for the treatment of age-related diseases.
MeSH term(s)	Animals ; Apoptosis ; Autophagosomes ; Autophagy ; Azocines/antagonists & inhibitors ; Benzhydryl Compounds/antagonists & inhibitors ; Cell Cycle ; Cell Proliferation ; Cellular Senescence/physiology ; Disease Models, Animal ; Gene Expression Regulation ; Inhibitor of Apoptosis Proteins/genetics ; Inhibitor of Apoptosis Proteins/metabolism ; Lysosomes ; Osteoarthritis/metabolism ; Osteoarthritis/pathology ; Qa-SNARE Proteins/metabolism ; Rats ; Rats, Sprague-Dawley ; Risk Factors
Chemical Substances	Azocines ; Benzhydryl Compounds ; Inhibitor of Apoptosis Proteins ; N-benzhydryl-5-(2-(methylamino)propanamido)-3-(3-methylbutanoyl)-6-oxodecahydropyrrolo(1,2-a)(1,5)diazocine-8-carboxamide ; Qa-SNARE Proteins ; Xiap protein, rat
Language	English
Publishing date	2019-06-26
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	60-7
ISSN	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbadis.2019.05.017
Database	MEDical Literature Analysis and Retrieval System OnLINE

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