File Download
Links for fulltext
(May Require Subscription)
- Publisher Website: 10.1002/jcp.29323
- Scopus: eid_2-s2.0-85074585092
- PMID: 31643095
- WOS: WOS:000491560500001
- Find via
Supplementary
- Citations:
- Appears in Collections:
Article: IL‐17 alters the mesenchymal stem cell niche towards osteogenesis in cooperation with osteocytes
Title | IL‐17 alters the mesenchymal stem cell niche towards osteogenesis in cooperation with osteocytes |
---|---|
Authors | |
Keywords | interleukin‐17 mesenchymal stem cells osteocytes osteogenesis |
Issue Date | 2020 |
Publisher | John Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/31010 |
Citation | Journal of Cellular Physiology, 2020, v. 235 n. 5, p. 4466-4480 How to Cite? |
Abstract | Bone remodeling is a strictly regulated dynamic process that cycles between bone formation and resorption, and interleukin‐17 (IL‐17) critically orchestrates the activation and differentiation of both osteoblasts and osteoclasts. Mesenchymal stem cells (MSCs) within their native environment receive biochemical stimuli from surrounding cells that influences their differentiation into bone precursors, while the roles of osteocytes in regulating the osteogenic differentiation of MSCs remain unclear. This study investigated the specific roles of IL‐17 signaling cascades and osteocyte‐specific pathways in the osteogenesis of MSCs. Using a transwell coculture (CC) system, we explored the effects of osteocytes and osteoblasts on the osteogenesis of MSCs with and without IL‐17 supplementation. A polycaprolactone (PCL) three‐dimensional (3D) culture model was used to evaluate their osteogenic potential in the presence of osteocytes and IL‐17. Notably, IL‐17 induced osteogenesis in MSCs, which could be attenuated by blocking IL‐17 receptor A. The osteogenic differentiation of MSCs promoted by IL‐17 was further enhanced by CC with osteocytes. Moreover, proinflammatory cytokines IL‐6 and IL‐1β played an important role in IL‐17‐dependent differentiation, via the phosphorylation of AKT, signal transducer and activator of transcription 3, and extracellular signal‐regulated kinase 1/2 signaling pathways in the MSC niche. The present study confirms a synergistic effect of osteocytes and IL‐17 in the production of biochemical signals to stimulate the osteogenic differentiation of MSCs, which could be further promoted in the PCL 3D‐scaffold. These findings provide important insight into the mechanisms of MSCs activation and osteogenic differentiation within the native stem cell niche, and suggest a possible role of IL‐17 in bone tissue engineering. |
Persistent Identifier | http://hdl.handle.net/10722/288020 |
ISSN | 2023 Impact Factor: 4.5 2023 SCImago Journal Rankings: 1.321 |
PubMed Central ID | |
ISI Accession Number ID |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | LIAO, C | - |
dc.contributor.author | Zhang, C | - |
dc.contributor.author | Jin, L | - |
dc.contributor.author | Yang, Y | - |
dc.date.accessioned | 2020-10-05T12:06:41Z | - |
dc.date.available | 2020-10-05T12:06:41Z | - |
dc.date.issued | 2020 | - |
dc.identifier.citation | Journal of Cellular Physiology, 2020, v. 235 n. 5, p. 4466-4480 | - |
dc.identifier.issn | 0021-9541 | - |
dc.identifier.uri | http://hdl.handle.net/10722/288020 | - |
dc.description.abstract | Bone remodeling is a strictly regulated dynamic process that cycles between bone formation and resorption, and interleukin‐17 (IL‐17) critically orchestrates the activation and differentiation of both osteoblasts and osteoclasts. Mesenchymal stem cells (MSCs) within their native environment receive biochemical stimuli from surrounding cells that influences their differentiation into bone precursors, while the roles of osteocytes in regulating the osteogenic differentiation of MSCs remain unclear. This study investigated the specific roles of IL‐17 signaling cascades and osteocyte‐specific pathways in the osteogenesis of MSCs. Using a transwell coculture (CC) system, we explored the effects of osteocytes and osteoblasts on the osteogenesis of MSCs with and without IL‐17 supplementation. A polycaprolactone (PCL) three‐dimensional (3D) culture model was used to evaluate their osteogenic potential in the presence of osteocytes and IL‐17. Notably, IL‐17 induced osteogenesis in MSCs, which could be attenuated by blocking IL‐17 receptor A. The osteogenic differentiation of MSCs promoted by IL‐17 was further enhanced by CC with osteocytes. Moreover, proinflammatory cytokines IL‐6 and IL‐1β played an important role in IL‐17‐dependent differentiation, via the phosphorylation of AKT, signal transducer and activator of transcription 3, and extracellular signal‐regulated kinase 1/2 signaling pathways in the MSC niche. The present study confirms a synergistic effect of osteocytes and IL‐17 in the production of biochemical signals to stimulate the osteogenic differentiation of MSCs, which could be further promoted in the PCL 3D‐scaffold. These findings provide important insight into the mechanisms of MSCs activation and osteogenic differentiation within the native stem cell niche, and suggest a possible role of IL‐17 in bone tissue engineering. | - |
dc.language | eng | - |
dc.publisher | John Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/31010 | - |
dc.relation.ispartof | Journal of Cellular Physiology | - |
dc.rights | This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. | - |
dc.subject | interleukin‐17 | - |
dc.subject | mesenchymal stem cells | - |
dc.subject | osteocytes | - |
dc.subject | osteogenesis | - |
dc.title | IL‐17 alters the mesenchymal stem cell niche towards osteogenesis in cooperation with osteocytes | - |
dc.type | Article | - |
dc.identifier.email | Zhang, C: zhangcf@hku.hk | - |
dc.identifier.email | Jin, L: ljjin@hkucc.hku.hk | - |
dc.identifier.email | Yang, Y: yangyanq@hku.hk | - |
dc.identifier.authority | Zhang, C=rp01408 | - |
dc.identifier.authority | Jin, L=rp00028 | - |
dc.identifier.authority | Yang, Y=rp00045 | - |
dc.description.nature | published_or_final_version | - |
dc.identifier.doi | 10.1002/jcp.29323 | - |
dc.identifier.pmid | 31643095 | - |
dc.identifier.pmcid | PMC7113695 | - |
dc.identifier.scopus | eid_2-s2.0-85074585092 | - |
dc.identifier.hkuros | 315357 | - |
dc.identifier.volume | 235 | - |
dc.identifier.issue | 5 | - |
dc.identifier.spage | 4466 | - |
dc.identifier.epage | 4480 | - |
dc.identifier.isi | WOS:000491560500001 | - |
dc.publisher.place | United States | - |
dc.identifier.issnl | 0021-9541 | - |