Effect of High-Dose Vitamin C on Tendon Cell Degeneration-An In Vitro Study
Tendinopathy is an aging-related disease, often caused by micro-scarring and degeneration due to overuse or trauma. Ascorbic acid (vitamin C) supplementation is reported to be a useful treatment for tendinopathy recovery. We compared the inhibitory effects of various ascorbic acid doses on tendon ce...
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| Veröffentlicht in: | International journal of molecular sciences 2024-12, Vol.25 (24), p.13358 |
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| creator | Ueda, Shusuke Ichiseki, Toru Shimasaki, Miyako Soma, Daisuke Sakurai, Masaru Kaneuji, Ayumi Kawahara, Norio |
| description | Tendinopathy is an aging-related disease, often caused by micro-scarring and degeneration due to overuse or trauma. Ascorbic acid (vitamin C) supplementation is reported to be a useful treatment for tendinopathy recovery. We compared the inhibitory effects of various ascorbic acid doses on tendon cell damage. H
O
was added to human-derived tendon cells in vitro (Group H
O
, control), followed by incubation with 150 µM or 30 mM of ascorbic acid (Group C, Group HC). The oxidative injury degree was evaluated by determining reactive oxygen species levels. The cytoskeletal structure was examined via fluorescence immunostaining of actin filaments. Quantitative polymerase chain reaction (qPCR) was performed to analyze the expressions of mitochondria transcription factor A, adenosine triphosphate 5A, type I collagen, and p16. Cell death was reduced, and oxidative stress was inhibited in C and HC groups. The cytoskeleton was maintained in the HC group but not in the C group. qPCR analysis revealed that p16 expression was inhibited in both the C and HC groups compared to the H
O
group; other markers had increased expression. The progression of cell death and cytoskeletal disruption was inhibited by the administration of high-dose vitamin C. Hence, high-dose vitamin C is a potential treatment for tendon cell degeneration. |
| doi_str_mv | 10.3390/ijms252413358 |
| format | Article |
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O
was added to human-derived tendon cells in vitro (Group H
O
, control), followed by incubation with 150 µM or 30 mM of ascorbic acid (Group C, Group HC). The oxidative injury degree was evaluated by determining reactive oxygen species levels. The cytoskeletal structure was examined via fluorescence immunostaining of actin filaments. Quantitative polymerase chain reaction (qPCR) was performed to analyze the expressions of mitochondria transcription factor A, adenosine triphosphate 5A, type I collagen, and p16. Cell death was reduced, and oxidative stress was inhibited in C and HC groups. The cytoskeleton was maintained in the HC group but not in the C group. qPCR analysis revealed that p16 expression was inhibited in both the C and HC groups compared to the H
O
group; other markers had increased expression. The progression of cell death and cytoskeletal disruption was inhibited by the administration of high-dose vitamin C. Hence, high-dose vitamin C is a potential treatment for tendon cell degeneration.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms252413358</identifier><identifier>PMID: 39769123</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Acids ; Aging ; Antioxidants ; Antioxidants - pharmacology ; Apoptosis ; Ascorbic Acid - pharmacology ; Autophagy ; Cell culture ; Cell cycle ; Cell death ; Cells, Cultured ; Collagen ; Comparative analysis ; Cyclin-dependent kinases ; Cytoskeleton ; Cytoskeleton - drug effects ; Cytoskeleton - metabolism ; Extracellular matrix ; Fluorescence ; Humans ; Hydrogen Peroxide - pharmacology ; Kinases ; Morphology ; Muscle proteins ; Oxidative stress ; Oxidative Stress - drug effects ; Physiological aspects ; Reactive Oxygen Species - metabolism ; Rotator cuff ; Senescence ; Tendinopathy - drug therapy ; Tendinopathy - metabolism ; Tendinopathy - pathology ; Tendons ; Tendons - drug effects ; Tendons - metabolism ; Tendons - pathology ; Trauma ; Vitamin C</subject><ispartof>International journal of molecular sciences, 2024-12, Vol.25 (24), p.13358</ispartof><rights>COPYRIGHT 2024 MDPI AG</rights><rights>2024 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c313t-9894415fa35058ee341df6eb53316e92f5be94ed02948ab02da956ae068ce4df3</cites><orcidid>0000-0001-7224-0722 ; 0000-0003-3385-032X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39769123$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ueda, Shusuke</creatorcontrib><creatorcontrib>Ichiseki, Toru</creatorcontrib><creatorcontrib>Shimasaki, Miyako</creatorcontrib><creatorcontrib>Soma, Daisuke</creatorcontrib><creatorcontrib>Sakurai, Masaru</creatorcontrib><creatorcontrib>Kaneuji, Ayumi</creatorcontrib><creatorcontrib>Kawahara, Norio</creatorcontrib><title>Effect of High-Dose Vitamin C on Tendon Cell Degeneration-An In Vitro Study</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>Tendinopathy is an aging-related disease, often caused by micro-scarring and degeneration due to overuse or trauma. Ascorbic acid (vitamin C) supplementation is reported to be a useful treatment for tendinopathy recovery. We compared the inhibitory effects of various ascorbic acid doses on tendon cell damage. H
O
was added to human-derived tendon cells in vitro (Group H
O
, control), followed by incubation with 150 µM or 30 mM of ascorbic acid (Group C, Group HC). The oxidative injury degree was evaluated by determining reactive oxygen species levels. The cytoskeletal structure was examined via fluorescence immunostaining of actin filaments. Quantitative polymerase chain reaction (qPCR) was performed to analyze the expressions of mitochondria transcription factor A, adenosine triphosphate 5A, type I collagen, and p16. Cell death was reduced, and oxidative stress was inhibited in C and HC groups. The cytoskeleton was maintained in the HC group but not in the C group. qPCR analysis revealed that p16 expression was inhibited in both the C and HC groups compared to the H
O
group; other markers had increased expression. The progression of cell death and cytoskeletal disruption was inhibited by the administration of high-dose vitamin C. Hence, high-dose vitamin C is a potential treatment for tendon cell degeneration.</description><subject>Acids</subject><subject>Aging</subject><subject>Antioxidants</subject><subject>Antioxidants - pharmacology</subject><subject>Apoptosis</subject><subject>Ascorbic Acid - pharmacology</subject><subject>Autophagy</subject><subject>Cell culture</subject><subject>Cell cycle</subject><subject>Cell death</subject><subject>Cells, Cultured</subject><subject>Collagen</subject><subject>Comparative analysis</subject><subject>Cyclin-dependent kinases</subject><subject>Cytoskeleton</subject><subject>Cytoskeleton - drug effects</subject><subject>Cytoskeleton - metabolism</subject><subject>Extracellular matrix</subject><subject>Fluorescence</subject><subject>Humans</subject><subject>Hydrogen Peroxide - pharmacology</subject><subject>Kinases</subject><subject>Morphology</subject><subject>Muscle proteins</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Physiological aspects</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Rotator cuff</subject><subject>Senescence</subject><subject>Tendinopathy - drug therapy</subject><subject>Tendinopathy - metabolism</subject><subject>Tendinopathy - pathology</subject><subject>Tendons</subject><subject>Tendons - drug effects</subject><subject>Tendons - metabolism</subject><subject>Tendons - pathology</subject><subject>Trauma</subject><subject>Vitamin C</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNptkc1LAzEQxYMo1q-jVwl48bKaZJLt5ljaqkXBgx_XJd2d1JRuosnuof-9W_wWmcMbht8bHjxCjjk7B9Dswi2bJJSQHEAVW2SPSyEyxvLh9o99QPZTWjImQCi9Swagh7nmAvbIzdRarFoaLL12i-dsEhLSJ9eaxnk6psHTB_R1L2NcregEF-gxmtYFn408nfkNGwO9b7t6fUh2rFklPPrQA_J4OX0YX2e3d1ez8eg2q4BDm-lCS8mVNaCYKhBB8trmOFcAPEctrJqjllgzoWVh5kzURqvcIMuLCmVt4YCcvf99ieG1w9SWjUtVn894DF0qgSsohkwL3aOnf9Bl6KLv0_WU1LliObBvamFWWDpvQxtNtXlajgrBC5BSb6jzf6h-amxcFTxa199_GbJ3QxVDShFt-RJdY-K65KzclFf-Kq_nTz7CdvMG6y_6sy14AzvakKA</recordid><startdate>20241212</startdate><enddate>20241212</enddate><creator>Ueda, Shusuke</creator><creator>Ichiseki, Toru</creator><creator>Shimasaki, Miyako</creator><creator>Soma, Daisuke</creator><creator>Sakurai, Masaru</creator><creator>Kaneuji, Ayumi</creator><creator>Kawahara, Norio</creator><general>MDPI AG</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-7224-0722</orcidid><orcidid>https://orcid.org/0000-0003-3385-032X</orcidid></search><sort><creationdate>20241212</creationdate><title>Effect of High-Dose Vitamin C on Tendon Cell Degeneration-An In Vitro Study</title><author>Ueda, Shusuke ; Ichiseki, Toru ; Shimasaki, Miyako ; Soma, Daisuke ; Sakurai, Masaru ; Kaneuji, Ayumi ; Kawahara, Norio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c313t-9894415fa35058ee341df6eb53316e92f5be94ed02948ab02da956ae068ce4df3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Acids</topic><topic>Aging</topic><topic>Antioxidants</topic><topic>Antioxidants - pharmacology</topic><topic>Apoptosis</topic><topic>Ascorbic Acid - pharmacology</topic><topic>Autophagy</topic><topic>Cell culture</topic><topic>Cell cycle</topic><topic>Cell death</topic><topic>Cells, Cultured</topic><topic>Collagen</topic><topic>Comparative analysis</topic><topic>Cyclin-dependent kinases</topic><topic>Cytoskeleton</topic><topic>Cytoskeleton - drug effects</topic><topic>Cytoskeleton - metabolism</topic><topic>Extracellular matrix</topic><topic>Fluorescence</topic><topic>Humans</topic><topic>Hydrogen Peroxide - pharmacology</topic><topic>Kinases</topic><topic>Morphology</topic><topic>Muscle proteins</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Physiological aspects</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Rotator cuff</topic><topic>Senescence</topic><topic>Tendinopathy - drug therapy</topic><topic>Tendinopathy - metabolism</topic><topic>Tendinopathy - pathology</topic><topic>Tendons</topic><topic>Tendons - drug effects</topic><topic>Tendons - metabolism</topic><topic>Tendons - pathology</topic><topic>Trauma</topic><topic>Vitamin C</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ueda, Shusuke</creatorcontrib><creatorcontrib>Ichiseki, Toru</creatorcontrib><creatorcontrib>Shimasaki, Miyako</creatorcontrib><creatorcontrib>Soma, Daisuke</creatorcontrib><creatorcontrib>Sakurai, Masaru</creatorcontrib><creatorcontrib>Kaneuji, Ayumi</creatorcontrib><creatorcontrib>Kawahara, Norio</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ueda, Shusuke</au><au>Ichiseki, Toru</au><au>Shimasaki, Miyako</au><au>Soma, Daisuke</au><au>Sakurai, Masaru</au><au>Kaneuji, Ayumi</au><au>Kawahara, Norio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of High-Dose Vitamin C on Tendon Cell Degeneration-An In Vitro Study</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2024-12-12</date><risdate>2024</risdate><volume>25</volume><issue>24</issue><spage>13358</spage><pages>13358-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>Tendinopathy is an aging-related disease, often caused by micro-scarring and degeneration due to overuse or trauma. Ascorbic acid (vitamin C) supplementation is reported to be a useful treatment for tendinopathy recovery. We compared the inhibitory effects of various ascorbic acid doses on tendon cell damage. H
O
was added to human-derived tendon cells in vitro (Group H
O
, control), followed by incubation with 150 µM or 30 mM of ascorbic acid (Group C, Group HC). The oxidative injury degree was evaluated by determining reactive oxygen species levels. The cytoskeletal structure was examined via fluorescence immunostaining of actin filaments. Quantitative polymerase chain reaction (qPCR) was performed to analyze the expressions of mitochondria transcription factor A, adenosine triphosphate 5A, type I collagen, and p16. Cell death was reduced, and oxidative stress was inhibited in C and HC groups. The cytoskeleton was maintained in the HC group but not in the C group. qPCR analysis revealed that p16 expression was inhibited in both the C and HC groups compared to the H
O
group; other markers had increased expression. The progression of cell death and cytoskeletal disruption was inhibited by the administration of high-dose vitamin C. Hence, high-dose vitamin C is a potential treatment for tendon cell degeneration.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>39769123</pmid><doi>10.3390/ijms252413358</doi><orcidid>https://orcid.org/0000-0001-7224-0722</orcidid><orcidid>https://orcid.org/0000-0003-3385-032X</orcidid><oa>free_for_read</oa></addata></record> |
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| source | MDPI - Multidisciplinary Digital Publishing Institute; MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Acids Aging Antioxidants Antioxidants - pharmacology Apoptosis Ascorbic Acid - pharmacology Autophagy Cell culture Cell cycle Cell death Cells, Cultured Collagen Comparative analysis Cyclin-dependent kinases Cytoskeleton Cytoskeleton - drug effects Cytoskeleton - metabolism Extracellular matrix Fluorescence Humans Hydrogen Peroxide - pharmacology Kinases Morphology Muscle proteins Oxidative stress Oxidative Stress - drug effects Physiological aspects Reactive Oxygen Species - metabolism Rotator cuff Senescence Tendinopathy - drug therapy Tendinopathy - metabolism Tendinopathy - pathology Tendons Tendons - drug effects Tendons - metabolism Tendons - pathology Trauma Vitamin C |
| title | Effect of High-Dose Vitamin C on Tendon Cell Degeneration-An In Vitro Study |
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