Search

Your search keyword '"Lim, Seongkyun"' showing total 37 results
Start Over Author "Lim, Seongkyun"
37 results on '"Lim, Seongkyun"'

2. Females display relatively preserved muscle quality compared with males during the onset and early stages of C26-induced cancer cachexia

Author

Cabrera, Ana Regina, primary, Deaver, J. William, additional, Lim, Seongkyun, additional, Morena da Silva, Francielly, additional, Schrems, Eleanor R., additional, Saling, Landen W., additional, Tsitkanou, Stavroula, additional, Rosa-Caldwell, Megan E., additional, Wiggs, Michael P., additional, Washington, Tyrone A., additional, and Greene, Nicholas P., additional

Published
2023
Full Text
View/download PDF

4. Development of skeletal muscle fibrosis in a rodent model of cancer cachexia

Author

Washington, Tyrone A., primary, Schrems, Eleanor R., additional, Haynie, Wesley S., additional, Rosa‐Caldwell, Megan E., additional, Brown, Jacob L., additional, Saling, Landen, additional, Lim, Seongkyun, additional, Perry, Richard A., additional, Brown, Lemuel A., additional, Lee, David E., additional, and Greene, Nicholas P., additional

Published
2023
Full Text
View/download PDF

6. A Rejuvenation Signature in Skeletal Muscle That Is Mediated By Late-Life Exercise

Author

Jones, Ronald, primary, Dimet-Wiley, Andrea, additional, Haghani, Amin, additional, Morena da Silva, Francielly, additional, Brightwell, Camille, additional, Lim, Seongkyun, additional, Khadgi, Sabin, additional, Wen, Yuan, additional, Dungan, Cory, additional, Brooke, Robert, additional, Greene, Nicholas, additional, Peterson, Charlotte, additional, McCarthy, John, additional, Horvath, Steve, additional, Watowich, Stanley, additional, Fry, Christopher, additional, and Murach, Kevin, additional

Published
2023
Full Text
View/download PDF

13. A molecular signature defining exercise adaptation with ageing and in vivo partial reprogramming in skeletal muscle

Author

Jones, Ronald G., primary, Dimet‐Wiley, Andrea, additional, Haghani, Amin, additional, da Silva, Francielly Morena, additional, Brightwell, Camille R., additional, Lim, Seongkyun, additional, Khadgi, Sabin, additional, Wen, Yuan, additional, Dungan, Cory M., additional, Brooke, Robert T., additional, Greene, Nicholas P., additional, Peterson, Charlotte A., additional, McCarthy, John J., additional, Horvath, Steve, additional, Watowich, Stanley J., additional, Fry, Christopher S., additional, and Murach, Kevin A., additional

Published
2023
Full Text
View/download PDF

25. Muscle miR-16 deletion results in impaired insulin sensitivity and contractile function in a sex-dependent manner

Author

Lim, Seongkyun, primary, Deaver, J. William, additional, Rosa-Caldwell, Megan E., additional, Lee, David E., additional, Morena da Silva, Francielly, additional, Cabrera, Ana Regina, additional, Schrems, Eleanor R., additional, Saling, Landen W., additional, Washington, Tyrone A., additional, Fluckey, James D., additional, and Greene, Nicholas P., additional

Published
2022
Full Text
View/download PDF

26. Development of metabolic and contractile alterations in development of cancer cachexia in female tumor-bearing mice

Author

Lim, Seongkyun, primary, Deaver, J. William, additional, Rosa-Caldwell, Megan E., additional, Haynie, Wesley S., additional, Morena da Silva, Francielly, additional, Cabrera, Ana Regina, additional, Schrems, Eleanor R., additional, Saling, Landen W., additional, Jansen, Lisa T., additional, Dunlap, Kirsten R., additional, Wiggs, Michael P., additional, Washington, Tyrone A., additional, and Greene, Nicholas P., additional

Published
2022
Full Text
View/download PDF

28. Female mice may have exacerbated catabolic signalling response compared to male mice during development and progression of disuse atrophy

Author

Rosa‐Caldwell, Megan E., primary, Lim, Seongkyun, additional, Haynie, Wesley A., additional, Brown, Jacob L., additional, Deaver, John William, additional, Morena Da Silva, Francielly, additional, Jansen, Lisa T., additional, Lee, David E., additional, Wiggs, Michael P., additional, Washington, Tyrone A., additional, and Greene, Nicholas P., additional

Published
2021
Full Text
View/download PDF

33. Sex Differences in Anabolic Regulators during Development of Atrophic Pathology in Hindlimb-Unloading-Induced Disuse

Author

Jansen, Lisa T., primary, Rosa-Caldwell, Megan E., additional, Haynie, Wesley S., additional, Lim, Seongkyun, additional, Dunlap, Kirsten, additional, Brown, Jacob L., additional, Lee, David E., additional, Perry, Richard A., additional, Wiggs, Michael P., additional, Washington, Tyrone A., additional, and Greene, Nicholas P., additional

Published
2019
Full Text
View/download PDF

35. Sex Differences in Cancer Cachexia and a Novel Mitochondrial Target for Cancer-Induced Muscle Wasting

Author

Lim, Seongkyun

Subjects
lewis lung carcinoma, mitochondria, muscle atrophy, OPA1, protein turnover, Biomechanics, Cancer Biology, Motor Control
Abstract

Cancer cachexia (CC) is a devastating wasting syndrome characterized by marked weight loss including skeletal muscle atrophy that affects approximately 80% of cancer patients. Current therapeutic treatments including pharmacological and nutritional intervention are insufficient to prevent or reverse it. Prior studies demonstrated lower muscle mass, impaired muscle function, and mitochondrial health in the development of CC. Specifically, mitochondrial fusion protein, Optic atrophy 1 (OPA1) which plays a significant role in skeletal muscle health, is suppressed in the development of CC. Furthermore, most pre-clinical CC studies were mainly focused on males although there are distinct phenotypical differences in skeletal muscle between males and females. Therefore, these studies were set to investigate two independent research questions (Chapter 3 & 4). The purpose of this dissertation project was to investigate skeletal muscle alterations during the development of CC in female tumor-bearing mice (Chapter 3) and determine the efficacy of OPA1 as a therapeutic target for cancer-induced muscle atrophy (Chapter 4). To accomplish this research plan, I completed a series of studies using both cell culture and animal models of CC. For the Chapter 3 experiments, 60 female mice were given either an IP injection of PBS or Lewis Lung Carcinoma (LLC) injection and the tumors were allowed to grow for 1, 2, 3, or 4-wk to assess the time course of cachectic development. We found a dichotomous effect on tumor mass between 3- and 4-wk animals where approximately half of mice between the two groups exhibited low tumor (LT) mass (2 g). Furthermore, HT mice revealed greater protein degradation, impaired muscle contractility, and mitochondrial degeneration. These alterations are relatively modest when compared to male data from previous studies. For the Chapter 4 experiments, I utilized both pharmacological (in vitro & in vivo) and genetic overexpression of OPA1 (OPA1 TG) in LLC-conditioned media (LCM) and LLC-induced CC. 72 hours of LCM intervention induced smaller myotubes, which was normalized by BGP-15 treatment and this effect appeared to be driven by suppressed inflammatory cytokine and autophagic-lysosomal pathway (ALP) activity at the mRNA level. 4-wk of LLC implantation was sufficient to induce cachectic phenotype while this effect was normalized in OPA1 overexpression in tumor-bearing mice. In conclusion, my dissertation data suggests both biological sex as an important variable and OPA1 as a novel therapeutic target for cancer-induced muscle wasting.

Published
2022

36. MicroRNA control of the myogenic cell transcriptome and proteome: the role of miR-16.

Author

Lim S, Lee DE, Morena da Silva F, Koopmans PJ, Vechetti IJ Jr, von Walden F, Greene NP, and Murach KA

Subjects
Cell Differentiation genetics, Muscle Development genetics, Muscle Fibers, Skeletal metabolism, Proteome genetics, Proteomics, Transcriptome genetics, Animals, Mice, MicroRNAs genetics, MicroRNAs metabolism
Abstract

MicroRNAs (miRs) control stem cell biology and fate. Ubiquitously expressed and conserved miR-16 was the first miR implicated in tumorigenesis. miR-16 is low in muscle during developmental hypertrophy and regeneration. It is enriched in proliferating myogenic progenitor cells but is repressed during differentiation. The induction of miR-16 blocks myoblast differentiation and myotube formation, whereas knockdown enhances these processes. Despite a central role for miR-16 in myogenic cell biology, how it mediates its potent effects is incompletely defined. In this investigation, global transcriptomic and proteomic analyses after miR-16 knockdown in proliferating C2C12 myoblasts revealed how miR-16 influences myogenic cell fate. Eighteen hours after miR-16 inhibition, ribosomal protein gene expression levels were higher relative to control myoblasts and p53 pathway-related gene abundance was lower. At the protein level at this same time point, miR-16 knockdown globally upregulated tricarboxylic acid (TCA) cycle proteins while downregulating RNA metabolism-related proteins. miR-16 inhibition induced specific proteins associated with myogenic differentiation such as ACTA2, EEF1A2, and OPA1. We extend prior work in hypertrophic muscle tissue and show that miR-16 is lower in mechanically overloaded muscle in vivo. Our data collectively point to how miR-16 is implicated in aspects of myogenic cell differentiation. A deeper understanding of the role of miR-16 in myogenic cells has consequences for muscle developmental growth, exercise-induced hypertrophy, and regenerative repair after injury, all of which involve myogenic progenitors.

Published
2023
Full Text
View/download PDF

37. Muscle miR-16 deletion results in impaired insulin sensitivity and contractile function in a sex-dependent manner.

Author

Lim S, Deaver JW, Rosa-Caldwell ME, Lee DE, Morena da Silva F, Cabrera AR, Schrems ER, Saling LW, Washington TA, Fluckey JD, and Greene NP

Subjects
Animals, Diet, High-Fat, Female, Glucose metabolism, Insulin metabolism, Male, Mice, Mice, Knockout, Muscle, Skeletal metabolism, Diabetes Mellitus, Type 2 genetics, Diabetes Mellitus, Type 2 metabolism, Glucose Intolerance genetics, Glucose Intolerance metabolism, Insulin Resistance genetics, MicroRNAs genetics, MicroRNAs metabolism
Abstract

microRNAs (miRs) are linked to various human diseases including type 2 diabetes mellitus (T2DM) and emerging evidence suggests that miRs may serve as potential therapeutic targets. Lower miR-16 content is consistent across different models of T2DM; however, the role of miR-16 in muscle metabolic health is still elusive. Therefore, the purpose of this study was to investigate how deletion of miR-16 in mice affects skeletal muscle metabolic health and contractile function in both sexes. This study was conducted using both 1 ) in vitro and 2 ) in vivo experiments. In in vitro experiments, we used C2C12 myoblasts to test if inhibition or overexpression of miR-16 affected insulin-mediated glucose handling. In in vivo experiments, we generated muscle-specific miR-16 knockout (KO) mice fed a high-fat diet (HFD) to assess how miR-16 content impacts metabolic and contractile properties including glucose tolerance, insulin sensitivity, muscle contractile function, protein anabolism, and mitochondrial network health. In in vitro experiments, although inhibition of miR-16 induced impaired insulin signaling ( P = 0.002) and glucose uptake ( P = 0.014), overexpression of miR-16 did not attenuate lipid overload-induced insulin resistance using the diacylglycerol analog 1-oleoyl-2-acetyl- sn -glycerol. In in vivo experiments, miR-16 deletion induced both impaired muscle contractility ( P = 0.031-0.033), and mitochondrial network health ( P = 0.008-0.018) in both sexes. However, although males specifically exhibited impaired insulin sensitivity following miR-16 deletion ( P = 0.030), female KO mice showed pronounced glucose intolerance ( P = 0.046), corresponding with lower muscle weights ( P = 0.015), and protein hyperanabolism ( P = 0.023). Our findings suggest distinct sex differences in muscle adaptation in response to miR-16 deletion and miR-16 may serve as a key regulator for metabolic dysregulation in T2DM. NEW & NOTEWORTHY We set to investigate the role of miR-16 in skeletal muscle during diet-induced insulin resistance. Our data provide novel evidence that the lack of miR-16 induced multiple aberrations in insulin sensitivity, muscle contractility, mitochondrial network health, and protein turnover in a sex-dependent manner. Interestingly, miR-16 deletion leads to insulin resistance in males and exacerbated glucose intolerance in females, suggesting different mechanisms of metabolic dysregulation with a lack of miR-16 between sexes.

Published
2022
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results