Steering the multipotent mesenchymal cells towards an anti-inflammatory and osteogenic bias via photobiomodulation therapy: How to kill two birds with one stone

Amaroli, Andrea; Pasquale, Claudio; Zekiy, Angelina Olegovna; Benedicenti, Stefano; Marchegiani, Andrea; Sabbieti, Maria Giovanna; Agas, Dimitrios

doi:10.1177/20417314221110192

Cited by 13 publications

(9 citation statements)

References 126 publications

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“…At 42 days, there was an increase in new bone formation and decrease in soft tissue volume in BCP group. Scientific studies have reported the positive effect of PBMT on the bone consolidation process by stimulating mitochondrial respiration, and increasing ATP synthesis, local blood flow, and collagen production, and consequently inducing proliferation and differentiation of osteoprogenitor cells [ 80 , 81 ].…”

Section: Discussionmentioning

confidence: 99%

Use of Photobiomodulation Combined with Fibrin Sealant and Bone Substitute Improving the Bone Repair of Critical Defects

et al. 2022

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In this preclinical protocol, an adjunct method is used in an attempt to overcome the limitations of conventional therapeutic approaches applied to bone repair of large bone defects filled with scaffolds. Thus, we evaluate the effects of photobiomodulation therapy (PBMT) on the bone repair process on defects filled with demineralized bovine bone (B) and fibrin sealant (T). The groups were BC (blood clot), BT (B + T), BCP (BC + PBMT), and BTP (B + T + PBMT). Microtomographically, BC and BCP presented a hypodense cavity with hyperdense regions adjacent to the border of the wound, with a slight increase at 42 days. BT and BTP presented discrete hyperdensing areas at the border and around the B particles. Quantitatively, BCP and BTP (16.96 ± 4.38; 17.37 ± 4.38) showed higher mean bone density volume in relation to BC and BT (14.42 ± 3.66; 13.44 ± 3.88). Histologically, BC and BCP presented deposition of immature bone at the periphery and at 42 days new bone tissue became lamellar with organized total collagen fibers. BT and BTP showed inflammatory infiltrate along the particles, but at 42 days, it was resolved, mainly in BTP. In the birefringence analysis, BT and BTP, the percentage of red birefringence increased (9.14% to 20.98% and 7.21% to 27.57%, respectively), but green birefringence was similar in relation to 14 days (3.3% to 3.5% and 3.5% to 4.2%, respectively). The number of osteocytes in the neoformed bone matrix proportionally reduced in all evaluated groups. Immunostaining of bone morphogenetic protein (BMP—2/4), osteocalcin (OCN), and vascular endothelial growth factor (VEGF) were higher in BCP and BTP when compared to the BC and BT groups (p < 0.05). An increased number of TRAP positive cells (tartrate resistant acid phosphatase) was observed in BT and BTP. We conclude that PBMT positively influenced the repair of bone defects filled with B and T.

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Section: Discussionmentioning

confidence: 99%

Use of Photobiomodulation Combined with Fibrin Sealant and Bone Substitute Improving the Bone Repair of Critical Defects

et al. 2022

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“…MSCs represent a significant therapeutic tool against a range of bone, bone marrow, and systemic inflammatory diseases due to their “hit‐and‐run” mode of action. This mechanism is based on exosomes and microvesicle production, and cytokines, chemokines, and other immunomodulatory factors release to quenching slow tissue “burn” and modulating inflammation (Amaroli et al, 2022; Wu et al, 2020). Certainly, there are multiple disease animal models where MSCs are believed to play a key role.…”

Section: Discussionmentioning

confidence: 99%

“…ANOVA, analysis of variance; CCL, chemokine (C-C motif) ligand; IL, interleukin; IFNγ, interferon-γ; GM-CSF, granulocyte-macrophage colony-stimulating factor; TNF-α, tumor necrosis factor-α; OVX, ovariectomized. immunomodulatory factors release to quenching slow tissue "burn" and modulating inflammation (Amaroli et al, 2022;Wu et al, 2020).…”

Section: Discussionmentioning

confidence: 99%

p62/SQSTM1 indirectly mediates remote multipotent mesenchymal cells and rescues bone loss and bone marrow integrity in ovariectomized rats

Agas

Marchegiani

Laus

et al. 2022

Journal Cellular Physiology

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Intramuscular administration of p62/SQSTM1 (sequestosome1)‐encoding plasmid demonstrated an anticancer effect in rodent models and dogs as well as a high safety profile and the first evidence of clinical benefits in humans. Also, an anti‐inflammatory effect of the plasmid was reported in several rodent disease models. Yet, the mechanisms of action for the p62 plasmid remain unknown. Here, we tested a hypothesis that the p62‐plasmid can act through the modulation of bone marrow multipotent mesenchymal cells (MSCs). We demonstrated that a p62 plasmid can affect MSCs indirectly by stimulating p62‐transfected cells to secrete an active ingredient(s) sensed by untransfected MSCs. When we transfected MSCs with the p62‐plasmid, collected their supernatant, and added it to an untransfected MSCs culture, it switched the differentiation state and prompt osteogenic responses of the untransfected MSCs. According to an accepted viewpoint, ovariectomy leads to bone pathology via dysregulation of MSCs, and restoring the MSC homeostasis would restore ovariectomy‐induced bone damage. To validate our in vitro observations in a clinically relevant in vivo model, we administered the p62 plasmid to ovariectomized rats. It partially reversed bone loss and notably reduced adipogenesis with concurrent reestablishing of the MSC subpopulation pool within the bone marrow. Overall, our study suggests that remote modulation of progenitor MSCs via administering a p62‐encoding plasmid may constitute a mechanism for its previously reported effects and presents a feasible disease‐preventing and/or therapeutic strategy.

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“…The bone marrow niche consists of multiple cell types, including hematopoietic stem cells, interacting with extracellular matrix, chemical, and physical factors, altogether forming the microenvironment responsible for maintaining blood cell formation (hematopoiesis) from development to adulthood [ 53 , 54 ]. In healthy normal development and maturation, the bone marrow niche regulates the fate and function of hematopoietic stem cells and their progeny primarily contributing to healthy aging [ 55 ].…”

Section: Tbi-induced Stem Cell Dysfunction: Potential Of Stem Cell-ba...mentioning

confidence: 99%

Stem Cell Therapy for Sequestration of Traumatic Brain Injury-Induced Inflammation

Borlongan

Rosi

2022

IJMS

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Traumatic brain injury (TBI) is one of the leading causes of long-term neurological disabilities in the world. TBI is a signature disease for soldiers and veterans, but also affects civilians, including adults and children. Following TBI, the brain resident and immune cells turn into a “reactive” state, characterized by the production of inflammatory mediators that contribute to the development of cognitive deficits. Other injuries to the brain, including radiation exposure, may trigger TBI-like pathology, characterized by inflammation. Currently there are no treatments to prevent or reverse the deleterious consequences of brain trauma. The recognition that TBI predisposes stem cell alterations suggests that stem cell-based therapies stand as a potential treatment for TBI. Here, we discuss the inflamed brain after TBI and radiation injury. We further review the status of stem cells in the inflamed brain and the applications of cell therapy in sequestering inflammation in TBI.

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Steering the multipotent mesenchymal cells towards an anti-inflammatory and osteogenic bias via photobiomodulation therapy: How to kill two birds with one stone

Cited by 13 publications

References 126 publications

Use of Photobiomodulation Combined with Fibrin Sealant and Bone Substitute Improving the Bone Repair of Critical Defects

Use of Photobiomodulation Combined with Fibrin Sealant and Bone Substitute Improving the Bone Repair of Critical Defects

p62/SQSTM1 indirectly mediates remote multipotent mesenchymal cells and rescues bone loss and bone marrow integrity in ovariectomized rats

Stem Cell Therapy for Sequestration of Traumatic Brain Injury-Induced Inflammation

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