The Implications of Brain-Derived Neurotrophic Factor in the Biological Activities of Platelet-Rich Plasma.
BDNF
PRP
inflammation
joint pain
osteoarthritis
platelets
Journal
Inflammation
ISSN: 1573-2576
Titre abrégé: Inflammation
Pays: United States
ID NLM: 7600105
Informations de publication
Date de publication:
21 Jun 2024
21 Jun 2024
Historique:
received:
24
03
2024
accepted:
31
05
2024
revised:
16
05
2024
medline:
21
6
2024
pubmed:
21
6
2024
entrez:
21
6
2024
Statut:
aheadofprint
Résumé
Platelet-rich plasma (PRP) is a biological blood-derived therapeutic obtained from whole blood that contains higher levels of platelets. PRP has been primarily used to mitigate joint degeneration and chronic pain in osteoarthritis (OA). This clinical applicability is based mechanistically on the release of several proteins by platelets that can restore joint homeostasis. Platelets are the primary source of brain-derived neurotrophic factor (BDNF) outside the central nervous system. Interestingly, BDNF and PRP share key biological activities with clinical applicability for OA management, such as anti-inflammatory, anti-apoptotic, and antioxidant. However, the role of BDNF in PRP therapeutic activities is still unknown. Thus, this work aimed to investigate the implications of BDNF in therapeutic outcomes provided by PRP therapy in vitro and in-vivo, using the MIA-OA animal model in male Wistar rats. Initially, the PRP was characterized, obtaining a leukocyte-poor-platelet-rich plasma (LP-PRP). Our assays indicated that platelets activated by Calcium release BDNF, and suppression of M1 macrophage polarization induced by LP-PRP depends on BDNF full-length receptor, Tropomyosin Kinase-B (TrkB). OA animals were given LP-PRP intra-articular and showed functional recovery in gait, joint pain, inflammation, and tissue damage caused by MIA. Immunohistochemistry for activating transcriptional factor-3 (ATF-3) on L4/L5 dorsal root ganglia showed the LP-PRP decreased the nerve injury induced by MIA. All these LP-PRP therapeutic activities were reversed in the presence of TrkB receptor antagonist. Our results suggest that the therapeutic effects of LP-PRP in alleviating OA symptoms in rats depend on BDNF/TrkB activity.
Identifiants
pubmed: 38904872
doi: 10.1007/s10753-024-02072-9
pii: 10.1007/s10753-024-02072-9
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Fundação de Amparo à Pesquisa do Estado de São Paulo
ID : 2018/10205-2
Organisme : Fundação de Amparo à Pesquisa do Estado de São Paulo
ID : 2018/10205-2
Organisme : Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
ID : 001
Informations de copyright
© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
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