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Background: We aimed to examine the accompanying and solo impacts of conditioned medium of human adipose-derived stem cells (h-ASC-COM) and photobiomodulation (PBM) on the maturation stage of an ischemic infected delayed-healing wound model (IIDHWM) of rats with type 2 diabetes (TIIDM). Results: Outcomes of the wound closure ratio (WCR) results, tensiometrical microbiological, and stereological assessment followed almost identical patterns. While the outcomes of h-ASC-COM + PBM, PBM only, and h-ASC-COM only regimes were significantly better for all evaluated methods than those of group 1(all, p < 0.001), PBM alone and h-ASC-COM + PBM therapy achieved superior results than h-ASC-COM only (ranged from p = 0.05 to p < 0.001). In terms of tensiometrical and stereological examinations, the results of h-ASC-COM + PBM experienced better results than the PBM only (all, p < 0.001). Conclusions: h-ASC-COM + PBM, PBM, and h-ASC-COM cures expressively accelerated the maturation stage in the wound healing process of IIDHWM with MRSA in TIIDM rats by diminishing the inflammatory reaction, and the microbial flora of MRSA; and increasing wound strength, WCR, number of fibroblasts, and new blood vessels. While the h-ASC-COM + PBM and PBM were more suitable than the effect of h-ASC-COM, the results of h-ASC-COM + PBM were superior to PBM only. [ABSTRACT FROM AUTHOR]

We investigated the impacts of photobiomodulation (PBM) and human allogeneic adipose-derived stem cells (ha-ADS) together and or alone applications on the stereological parameters, immunohistochemical characterizing of M1 and M2 macrophages, and mRNA levels of hypoxia-inducible factor (HIF-1α), basic fibroblast growth factor (bFGF), vascular endothelial growth factor-A (VEGF-A) and stromal cell-derived factor-1α (SDF-1α) on inflammation (day 4) and proliferation phases (day 8) of repairing tissues in an infected delayed healing and ischemic wound model (IDHIWM) in type 1 diabetic (DM1) rats. DM1 was created in 48 rats and an IDHIWM was made in all of them, and they were distributed into 4 groups. Group1 = control rats with no treatment. Group2 = rats received (10 × 100000 ha-ADS). Group3 = rats exposed to PBM (890 nm, 80 Hz, 3.46 J/cm2). Group4 = rats received both PBM and ha-ADS. On day 8, there were significantly higher neutrophils in the control group than in other groups (p < 0.01). There were substantially higher macrophages in the PBM + ha-ADS group than in other groups on days 4 and 8 (p < 0.001). Granulation tissue volume, on both days 4 and 8, was meaningfully greater in all treatment groups than in the control group (all, p = 0.000). Results of M1 and M2 macrophage counts of repairing tissue in the entire treatment groups were considered preferable to those in the control group (p < 0.05). Regarding stereological and macrophage phenotyping, the results of the PBM + ha-ADS group were better than the ha-ADS and PBM groups. Results of the tested gene expression of repairing tissue on inflammation and proliferation steps in PBM and PBM + ha-ADS groups were meaningfully better than the control and ha-ADS groups (p < 0.05). We showed that PBM, ha-ADS, and PBM plus ha-ADS, hastened the proliferation step of healing in an IDHIWM in rats with DM1 by regulation of the inflammatory reaction, macrophage phenotyping, and augmented granulation tissue formation. In addition PBM and PBM plus ha-ADS protocols hastened and increased mRNA levels of HIF-1α, bFGF, SDF-1α, and VEGF-A. Totally, in terms of stereological and immuno-histological tests, and also gene expression HIF-1α and VEGF-A, the results of PBM + ha-ADS were superior (additive) to PBM, and ha-ADS alone treatments. [ABSTRACT FROM AUTHOR]

This document is a correction notice for an article titled "Photobiomodulation preconditioned diabetic adipose derived stem cells with additional photobiomodulation: an additive approach for enhanced wound healing in diabetic rats with a delayed healing wound" published in the journal Lasers in Medical Science. The correction states that Figures 3 and 4 in the original article were mistakenly swapped and have been corrected. The publisher, Springer Nature, remains neutral regarding jurisdictional claims and institutional affiliations. The authors of the article are listed as Dorsa Vatandoust, Houssein Ahmadi, Abdollah Amini, Atarodalsadat Mostafavinia, Fadaei Fatemeh Fathabady, Ali Moradi, Mohammadjavad Fridoni, Michael R Hamblin, Roohollah Ebrahimpour-Malekshah, Sufan Chien, and Mohammad Bayat. [Extracted from the article]

[Display omitted] • Photobiomodulation (PBM) may be able to improve function of diabetic stem cell. • PBM increases cell viability, and gene expression of antioxidant agents. • PBM decreases population doubling time, apoptosis, and ROS. • PBM decreases gene expression of oxidative stress biomarkers. We studied the effects of photobiomodulation therapy (PBMT) on adipose-derived mesenchymal stem cells (ADSCs) which were extracted from streptozotocin (STZ) induced diabetic rats. Adipose tissue was extracted from the hypodermis of diabetic rats, and diabetic ADSCs were extracted, characterized, and cultured. There were two in vitro groups: control-diabetic ADSCs, and PBMT-diabeticADSCs. We used 630 nm and 810 nm laser at 1.2 J/cm2 with 3 applications 48 h apart. We measured cell viability, apoptosis, population doubling time (PDT), and reactive oxygen species (ROS) by flow cytometry. Gene expression of antioxidants, including cytosolic copper-zinc superoxide dismutase (SOD1), catalase (CAT), total antioxidant capacity (TAC), and oxidative stress biomarkers (NADPH oxidase 1 and 4) by quantitative real time (qRT) - PCR. In this study, data were analyzed using t -test. Viability of PBMT-diabetic- ADSC group was higher than control- diabetic-ADSC (p = 0.000). PDT and apoptosis of PBMT- diabetic-ADSC group were lower than control-diabetic -ADSC (p = 0.001, p = 0.02). SOD1 expression and TAC of PBMT- diabetic-ADSC group were higher than control –diabetic -ADSC (p = 0.018, p = 0.005). CAT of PBMT –diabetic-ADSC group was higher than control-diabetic -ADSC. ROS, NOX1, and NOX4 of PBMT- diabetic -ADSC group were lower than control-diabetic-ADSC (p = 0.002, p = 0.021, p = 0.017). PBMT may improve diabetic- ADSC function in vitro by increasing levels of cell viability, and gene expression of antioxidant agents (SOD1, CAT, and TAC), and significantly decreasing of levels of PDT, apoptosis, ROS, and gene expression of oxidative stress biomarkers (NOX1 and NOX4). [ABSTRACT FROM AUTHOR]

Highlights • Grafted Sertoli cells (SCs) exhibited a decline in apoptosis in a rat model of amyloid beta toxicity. • Implantation of SCs in rats with Aβ1-42 receiving vehicle decreased the amount of gliosis. • We found that implanted SCs can recover hippocampus dependent memory and learning. • Transplanted SCs restored long-term synaptic plasticity in lesioned rats. Abstract Alzheimer's disease (AD) is a degenerative nerve disease which adversely affects memory and learning skills. Currently, there is no disease-modifying therapeutic approach for AD. However, a growing body of literature suggests cell based therapies as a promising remedy for neurological disorders. Among the potential cell sources, testis- derived Sertoli cells (SCs) appear to be an attractive choice due to their immune-privileged capacities. Herein, we investigated the neuro-restorative/protective effects of SC transplants in a rat model of amyloid beta toxicity. To this end, GATA-4 and vimentin positive SCs were transplanted into rats with amyloid beta induced hippocampal lesions. According to our in vivo results, implanted SCs survived, exhibited reduction in both apoptosis as well as astrocytic migration. Additionally, transplantation of SCs restored hippocampus dependent memory and learning, along with the recovery of long-term synaptic plasticity. Taken together, these data indicate that SCs are a valuable source for cell-based therapies particularly aimed at AD. [ABSTRACT FROM AUTHOR]

[Display omitted] • Photobiomodulation improved ATP quantity in diabetic-stem cells related to the control ones. • Photobiomodulation increased MMP activity in diabetic-stem cells compared to the control ones. • Photobiomodulation(PBM) decreased ROS, PINK1 and PARKIN gene expression of diabetic stem cells. • PBM marinates function of mitochondrial diabetic-stem cells. • PBM is an attractive agent for improving the efficacy of autologous diabetic stem cell. Herein are reported the effects of photobiomodulation (PBM) on adenosine triphosphate (ATP) and reactive oxygen species (ROS) quantification and mitochondria membrane potential (MMP) of the mitochondria of diabetic adipose-derived stem cells (ADSCs) in vitro. Additionally, the expression of PTEN-induced kinase 1 (PINK1) and RBR E3 ubiquitin-protein ligase (PARKIN) genes, which are involved in mitochondrial quality, were quantified. First, type one diabetes was induced in 10 rats. The rats were then kept for 1 month, after which fat tissue was excised from subcutaneous regions, and stem cells were selected from the fat, characterized as ADSC, and cultivated and increased in elevated sugar conditions in vitro; these samples were considered diabetic-ADSC. Two groups were formed, namely, diabetic-control-ADSC and PBM–diabetic-ADSC. ATP, ROS quantification, and MMP of mitochondria of diabetic ADSCs in vitro were measured, and the expression of PINK1 and Parkin genes was quantified in vitro. The results revealed that PBM significantly increased ATP quantification (p = 0.05) and MMP activity (p = 0.000) in diabetic-ADSCs in vitro compared to the control diabetic-ADSCs; however, it significantly decreased ROS quantification (p = 0.002) and PINK1(p = 0.003) and PARKIN gene expression (p = 0.046) in diabetic-ADSCs. The current findings indicate for the first time that PBM has the potential to maintain the function and quality of mitochondrial diabetic-ADSCs by significantly increasing ATP quantification and MMP activity in diabetic-ADSCs in vitro while significantly decreasing ROS quantification and PINK1 and PARKIN gene expression, making PBM an attractive candidate for use in improving the efficacy of autologous stem cell remedies for diabetic patients with infected diabetic foot ulcers. [ABSTRACT FROM AUTHOR]