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The Incidence of Serum Calcium Elevation due to Adrenal Insufficiency After Unilateral Adrenalectomy
Woochul Kim,Jee-Hye Choi,Ja Kyung Lee,Chang Ho Ahn,Hyeong Won Yu,June Young Choi 대한내분비외과학회 2022 The Koreran journal of Endocrine Surgery Vol.22 No.1
Purpose To investigate the incidence of elevated serum calcium levels after unilateral adrenalectomy. Methods A total of 239 patients who underwent unilateral adrenalectomy from March 2013 to April 2021 at Seoul National University Bundang Hospital were analyzed retrospectively for this study. The patients’ medical records were reviewed to identify changes in serum calcium levels. Calcium levels were corrected for analysis. Results Of 239 patients, 7.5% showed significant increases in the corrected serum calcium levels. In those patients, the glomerular filtration rate and serum albumin levels were decreased postoperatively. A single patient showed life-threatening hypercalcemia requiring re-admission. Conclusion Unilateral adrenalectomy may result in elevated serum calcium levels. These elevations might be partly due to adrenal insufficiency. A preoperative evaluation may be needed to prevent hypercalcemic events.
Anti-death strategies against oxidative stress in grafted mesenchymal stem cells.
Chang, Woochul,Song, Byeong-Wook,Moon, Jae-Youn,Cha, Min-Ji,Ham, Onju,Lee, Se-Yeon,Choi, Eunmi,Choi, Eunhyun,Hwang, Ki-Chul Gutenberg 2013 Histology and histopathology Vol.28 No.12
<P>Mesenchymal stem cells (MSCs) possess the potential for use in cell-based therapy for repair of myocardial injury. The therapeutic potential of MSCs is based on the capacity of MSCs to differentiate into cardiac tissue and release paracrine factors. However, a major problem in the clinical application of MSC-based therapy is the poor viability of transplanted MSCs at the site of graft due to harsh microenvironment conditions, such as ischemia and/or anoikis. Ischemia after myocardial infarction (MI) and interaction of MSCs with their niche is associated with increased production of reactive oxygen species (ROS). ROS hinder cell adhesion and induce detachment of cells, which induces anoikis signals in implanted MSCs. Therefore, strategies to regulate oxidative stress following the implantation of MSCs are therapeutically attractive. In this review, we first describe ROS as a major obstacle in MSC-based therapy and focus on manipulation of implanted MSCs to reduce ROS-mediated anoikis.</P>
Chang, Woochul,Kim, Ran,Park, Sang In,Jung, Yu Jin,Ham, Onju,Lee, Jihyun,Kim, Ji Hyeong,Oh, Sekyung,Lee, Min Young,Kim, Jongmin,Park, Moon-Seo,Chung, Yong-An,Hwang, Ki-Chul,Maeng, Lee-So Korean Society for Molecular and Cellular Biology 2015 Molecules and cells Vol.38 No.7
The use of conditioned medium from mesenchymal stem cells may be a feasible approach for regeneration of bone defects through secretion of various components of mesenchymal stem cells such as cytokines, chemokines, and growth factors. Mesenchymal stem cells secrete and accumulate multiple factors in conditioned medium under specific physiological conditions. In this study, we investigated whether the conditioned medium collected under hypoxic condition could effectively influence bone regeneration through enhanced migration and adhesion of endogenous mesenchymal stem cells. Cell migration and adhesion abilities were increased through overexpression of intercellular adhesion molecule-1 in hypoxic conditioned medium treated group. Intercellular adhesion molecule-1 was upregulated by microRNA-221 in mesenchymal stem cells because microRNAs are key regulators of various biological functions via gene expression. To investigate the effects in vivo, evaluation of bone regeneration by computed tomography and histological assays revealed that osteogenesis was enhanced in the hypoxic conditioned medium group relative to the other groups. These results suggest that behavioral changes of endogenous mesenchymal stem cells through microRNA-221 targeted-intercellular adhesion molecule-1 expression under hypoxic conditions may be a potential treatment for patients with bone defects.
Chang, Woochul,Song, Byeong-Wook,Lim, Soyeon,Song, Heesang,Shim, Chi Young,Cha, Min-Ji,Ahn, Dong Hyuck,Jung, Young-Gook,Lee, Dong-Ho,Chung, Ji Hyung,Choi, Ki-Doo,Lee, Seung-Kyou,Chung, Namsik,Lee, San AlphaMed Press 2009 Stem Cells Vol.27 No.9
<P>Mesenchymal stem cell (MSC) therapy for myocardial injury has inherent limitations due to the poor viability of MSCs after cell transplantation. In this study, we directly delivered Hsp70, a protein with protective functions against stress, into MSCs, using the Hph-1 protein transduction domain ex vivo for high transfection efficiency and low cytotoxicity. Compared to control MSCs in in vitro hypoxic conditions, MSCs delivered with Hph-1-Hsp70 (Hph-1-Hsp70-MSCs) displayed higher viability and anti-apoptotic properties, including Bcl2 increase, reduction of Bax, JNK phosphorylation and caspase-3 activity. Hsp70 delivery also attenuated cellular ATP-depleting stress. Eight animals per group were used for in vivo experiments after occlusion of the left coronary artery. Transplantation of Hph-1-Hsp70-MSCs led to a decrease in the fibrotic heart area, and significantly reduced the apoptotic positive index by 19.5 +/- 2%, compared to no-treatment controls. Hph-1-Hsp70-MSCs were well-integrated into the infarcted host myocardium. The mean microvessel count per field in the infarcted myocardium of the Hph-1-Hsp70-MSC-treated group (122.1 +/- 13.5) increased relative to the MSC-treated group (75.9 +/- 10.4). By echocardiography, transplantation of Hph-1-Hsp70-MSCs resulted in additional increases in heart function, compared to the MSCs-transplanted group. Our results may help formulate better clinical strategies for in vivo MSC cell therapy for myocardial damage.</P>
Therapeutic Potential of Stem Cells Strategy for Cardiovascular Diseases
Lee, Chang Youn,Kim, Ran,Ham, Onju,Lee, Jihyun,Kim, Pilseog,Lee, Seokyeon,Oh, Sekyung,Lee, Hojin,Lee, Minyoung,Kim, Jongmin,Chang, Woochul Hindawi Publishing Corporation 2016 Stem cells international Vol.2016 No.-
<P>Despite development of medicine, cardiovascular diseases (CVDs) are still the leading cause of mortality and morbidity worldwide. Over the past 10 years, various stem cells have been utilized in therapeutic strategies for the treatment of CVDs. CVDs are characterized by a broad range of pathological reactions including inflammation, necrosis, hyperplasia, and hypertrophy. However, the causes of CVDs are still unclear. While there is a limit to the currently available target-dependent treatments, the therapeutic potential of stem cells is very attractive for the treatment of CVDs because of their paracrine effects, anti-inflammatory activity, and immunomodulatory capacity. Various studies have recently reported increased therapeutic potential of transplantation of microRNA- (miRNA-) overexpressing stem cells or small-molecule-treated cells. In addition to treatment with drugs or overexpressed miRNA in stem cells, stem cell-derived extracellular vesicles also have therapeutic potential because they can deliver the stem cell-specific RNA and protein into the host cell, thereby improving cell viability. Here, we reported the state of stem cell-based therapy for the treatment of CVDs and the potential for cell-free based therapy.</P>
<i>Salvia miltiorrhiza</i> enhances the survival of mesenchymal stem cells under ischemic conditions
Kim, Ran,Lee, Seokyeon,Lee, Chang Youn,Yun, Hwayoung,Lee, Hojin,Lee, Min Young,Kim, Jongmin,Jeong, Jee‐,Yeong,Baek, Kyungmin,Chang, Woochul John Wiley and Sons Inc. 2018 Journal of pharmacy and pharmacology Vol.70 No.9
<P><B>Abstract</B></P><P><B>Objectives</B></P><P>To validate the enhanced therapeutic effect of <I>Salvia miltiorrhiza</I> Bunge (SM) for brain ischemic stroke through the anti‐apoptotic and survival ability of mesenchymal stem cells (MSCs).</P><P><B>Methods</B></P><P>The viability and the expression level of cell apoptotic and survival‐related proteins in MSCs by treatment of SM were assessed <I>in vitro</I>. In addition, the infarcted brain region and the behavioural changes after treatment of MSCs with SM were confirmed in rat middle cerebral artery occlusion (MCAo) models.</P><P><B>Key findings</B></P><P>We demonstrated that SM attenuates apoptosis and improves the cell viability of MSCs. In the rat MCAo model, the recovery of the infarcted region and positive changes of behaviour are observed after treatment of MSCs with SM.</P><P><B>Conclusions</B></P><P>The therapy using SM enhances the therapeutic effect for brain ischemic stroke by promoting the survival of MSCs. This synergetic effect thereby proposes a new experimental approach of traditional Chinese medicine and stem cell‐based therapies for patients suffering from a variety of diseases.</P>
Hypermethylation of PDX1, EN2, and MSX1 predicts the prognosis of colorectal cancer
Lee Yeongun,Dho So Hee,Lee Jiyeon,Hwang Ji-Hyun,Kim Minjung,Choi Won-Young,Lee Jin-Young,Lee Jongwon,Chang Woochul,Lee Min Young,Choi Jungmin,Kim Tae-You,Kim Lark Kyun 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-
Despite numerous observations regarding the relationship between DNA methylation changes and cancer progression, only a few genes have been verified as diagnostic biomarkers of colorectal cancer (CRC). To more practically detect methylation changes, we performed targeted bisulfite sequencing. Through co-analysis of RNA-seq, we identified cohort-specific DNA methylation markers: CpG islands of the intragenic regions of PDX1, EN2, and MSX1. We validated that these genes have oncogenic features in CRC and that their expression levels are increased in correlation with the hypermethylation of intragenic regions. The reliable depth of the targeted bisulfite sequencing data enabled us to design highly optimized quantitative methylation-specific PCR primer sets that can successfully detect subtle changes in the methylation levels of candidate regions. Furthermore, these methylation levels can divide CRC patients into two groups denoting good and poor prognoses. In this study, we present a streamlined workflow for screening clinically significant differentially methylated regions. Our discovery of methylation markers in the PDX1, EN2, and MSX1 genes suggests their promising performance as prognostic markers and their clinical application in CRC patients.
Song, Heesang,Chang, Woochul,Lim, Soyeon,Seo, Hye-Sun,Shim, Chi Young,Park, Sungha,Yoo, Kyung-Jong,Kim, Byung-Soo,Min, Byoung-Hyun,Lee, Hakbae,Jang, Yangsoo,Chung, Namsik,Hwang, Ki-Chul Wiley (John WileySons) 2007 Stem Cells Vol.25 No.6
<P>Autologous mesenchymal stem cell (MSC) transplantation therapy for repair of myocardial injury has inherent limitations due to the poor viability of the stem cells after cell transplantation. Adhesion is a prerequisite for cell survival and also a key factor for the differentiation of MSCs. As a novel prosurvival modification strategy, we genetically engineered MSCs to overexpress tissue transglutaminase (tTG), with intention to enhance adhesion and ultimately cell survival after implantation. tTG-transfected MSCs (tTG-MSCs) showed a 2.7-fold and greater than a twofold increase of tTG expression and surface tTG activity, respectively, leading to a 20% increased adhesion of MSCs on fibronectin (Fn). Spreading and migration of tTG-MSCs were increased 4.75% and 2.52%, respectively. Adhesion of tTG-MSCs on cardiogel, a cardiac fibroblast-derived three-dimensional matrix, showed a 33.1% increase. Downregulation of tTG by transfection of small interfering RNA specific to the tTG resulted in markedly decreased adhesion and spread of MSCs on Fn or cardiogel. tTG-MSCs on Fn significantly increased phosphorylation of focal adhesion related kinases FAK, Src, and PI3K. tTG-MSCs showed significant retention in infarcted myocardium by forming a focal adhesion complex and developed into cardiac myocyte-like cells by the expression of cardiac-specific proteins. Transplantation of 1 x 10(6) MSCs transduced with tTG into the ischemic rat myocardium restored normalized systolic and diastolic cardiac function. tTG-MSCs further restored cardiac function of infarcted myocardium as compared with MSC transplantation alone. These findings suggested that tTG may play an important role in integrin-mediated adhesion of MSCs in implanted tissues. Disclosure of potential conflicts of interest is found at the end of this article.</P>
PLCδ1 protein rescues ischemia-reperfused heart by the regulation of calcium homeostasis.
Lim, Soyeon,Chang, Woochul,Cha, Min-Ji,Song, Byeong-Wook,Ham, Onju,Lee, Se-Yeon,Lee, Changyoun,Park, Jun-Hee,Lee, Sang-Kyou,Jang, Yangsoo,Hwang, Ki-Chul Academic Press 2014 MOLECULAR THERAPY Vol.22 No.6
<P>Myocardial Ca(2+) overload induced by ischemia/reperfusion (I/R) is a major element of myocardial dysfunction in heart failure. Phospholipase C (PLC) plays important roles in the regulation of the phosphoinositol pathway and Ca(2+) homeostasis in various types of cells. Here, we investigated the protective role of PLCδ1 against myocardial I/R injury through the regulation of Ca(2+) homeostasis. To investigate its role, PLCδ1 was fused to Hph1, a cell-permeable protein transduction domain (PTD), and treated into rat neonatal cardiomyocytes and rat hearts under respective hypoxia-reoxygenation (H/R) and ischemia-reperfusion conditions. Treatment with Hph1-PLCδ1 significantly inhibited intracellular Ca(2+) overload, reactive oxygen species generation, mitochondrial permeability transition pore opening, and mitochondrial membrane potential elevation in H/R neonatal cardiomyocytes, resulting in the inhibition of apoptosis. Intravenous injections of Hph1-PLCδ1 in rats with I/R-injured myocardium caused significant reductions in infarct size and apoptosis and also improved systolic and diastolic cardiac functioning. Furthermore, a small ions profile obtained using time-of-flight secondary ion mass spectrometry showed that treatment with Hph1-PLCδ1 leads to significant recovery of calcium-related ions toward normal levels in I/R-injured myocardium. These results suggest that Hph1-PLCδ1 may manifest as a promising cardioprotective drug due to its inhibition of the mitochondrial apoptotic pathway in cells suffering from I/R injury.</P>