Studies on the effects of bone marrow stem cells on mitochondrial function and the alleviation of ARDS
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Studies on the effects of bone marrow stem cells on mitochondrial function and the alleviation of ARDS Keji Zhang1 · Yuan Gao2 · Yuxiao Deng2 · Xiao Zhou2 · Changqing Zhu1 · Zhengyu He2 · Dan Lv1 Received: 22 April 2020 / Accepted: 14 August 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Mesenchymal stem cells (MSCs) can alleviate acute respiratory distress syndrome (ARDS), but the mechanisms involved are unclear, especially about their specific effects on cellular mitochondrial respiratory function. Thirty mice were allocated into the Control, LPS, and LPS + Bone marrow mesenchymal stem cell (BMSC) group (n = 10/group). Mouse alveolar epithelial cells (MLE-12) and macrophage cells (RAW264.7) were divided into the same groups. Pathological variation, inflammationrelated factors, reactive oxygen species (ROS), ATP levels, and oxygen consumption rate (OCR) were analyzed. Pathologic features of ARDS were observed in the LPS group and were significantly alleviated by BMSCs. The trend in inflammationrelated factors among the three groups was the LPS group > LPS + BMSC group > Control group. In the MLE-12 co-culture system, IL-6 was increased in the LPS group but not significantly reduced in the LPS + BMSC group. In the RAW264.7 co-culture system, IL-1β, TNF-α, and IL-10 levels were all increased in the LPS group, IL-1β and TNF-α levels were reduced by BMSCs, while IL-10 level kept increasing. ROS and ATP levels were increased and decreased respectively in both MLE-12 and RAW264.7 cells in the LPS groups but reversed by BMSCs. Basal OCR, ATP-linked OCR, and maximal OCR were lower in the LPS groups. Impaired basal OCR and ATP-linked OCR in MLE-12 cells were partially restored by BMSCs, while impaired basal OCR and maximal OCR in RAW264.7 cells were restored by BMSCs. BMSCs improved the mitochondrial respiration dysfunction of macrophages and alveolar epithelial cells induced by LPS, alleviated lung tissue injury, and inflammatory response in a mouse model of ARDS. Keywords BMSCs · ARDS · Macrophages · Alveolar epithelial cells · Mitochondrial respiratory function · OCR
Introduction Acute respiratory distress syndrome (ARDS) is the leading cause of death in ICU patients [1]. ARDS is a severe complication of patients presenting life-threatening organ dysfunction caused by a dysregulated host response to viral (e.g., SARS-CoV-2), bacterial, or fungal infection [2], and about 67% of patients with COVID-19 admitted to the ICU * Yuan Gao [email protected] * Yuxiao Deng [email protected] 1
Department of Emergency, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, China
Department of Critical Care Medicine, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, China
2
are diagnosed with ARDS [3]. As a multifactorial syndrome, ARDS involves severe lung injury characterized by hypoxemia, loss of lung compliance, and pulmonary edema [4]. The pathology of ARDS is strongly associated with pulmonary sepsis and can invol
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