Cellular prion protein activates Caspase 3 for apoptotic defense mechanism in astrocytes
The cellular prion protein (PrP C ) is anchored in the plasma membrane of cells, and it is highly present in cells of brain tissue, exerting numerous cellular and cognitive functions. The present study proves the importance of PrP C in the cellular defense mechanism and metal homeostasis in astrocyt...
Gespeichert in:
| Veröffentlicht in: | Molecular and cellular biochemistry 2021-05, Vol.476 (5), p.2149-2158 |
|---|---|
| Hauptverfasser: | , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 2158 |
|---|---|
| container_issue | 5 |
| container_start_page | 2149 |
| container_title | Molecular and cellular biochemistry |
| container_volume | 476 |
| creator | Marques, Caroline M. S. Pedron, Tatiana Batista, Bruno L. Cerchiaro, Giselle |
| description | The cellular prion protein (PrP
C
) is anchored in the plasma membrane of cells, and it is highly present in cells of brain tissue, exerting numerous cellular and cognitive functions. The present study proves the importance of PrP
C
in the cellular defense mechanism and metal homeostasis in astrocytes cells. Through experimental studies using cell lines of immortalized mice astrocytes (wild type and knockout for PrP
C
), we showed that PrPc is involved in the apoptosis cell death process by the activation of Caspase 3, downregulation of p53, and cell cycle maintenance. Metal homeostasis was determined by inductively coupled plasma mass spectrometry technique, indicating the crucial role of PrP
C
to lower intracellular calcium. The lowered calcium concentration and the Caspase 3 downregulation in the PrP
C
-null astrocytes resulted in a faster growth rate in cells, comparing with PrP
C
wild-type one. The presence of PrP
C
shows to be essential to cell death and healthy growth. In conclusion, our results show for the first time that astrocyte knockout cells for the cellular prion protein could modulate apoptosis-dependent cell death pathways.
Graphic abstract |
| doi_str_mv | 10.1007/s11010-021-04078-5 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_2487156654</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A659190587</galeid><sourcerecordid>A659190587</sourcerecordid><originalsourceid>FETCH-LOGICAL-c442t-a4c22b15aab3fe48319f368e7bee080a5c5d2a7d3efa5358f38f1738356068733</originalsourceid><addsrcrecordid>eNp9kd9rFDEQx4Mo9jz9B3yQBV982Zqfm9xjOdQKBV9a6FvIZSc1ZTc5k6zQ_965XmtRRBISmHy-k5n5EvKW0VNGqf5YGaOM9pSznkqqTa-ekRVTWvRywzbPyYoKSnvDtD4hr2q9pUhTxl6SEyGU1LhX5HoL07RMrnT7EnPCMzeIqXO-xZ-uQe22ru5dhU50IZfO7fO-5RZ9N0KAhPEZ_HeXYp27g6y2kv0d6l6TF8FNFd483Gty9fnT5fa8v_j25ev27KL3UvLWO-k53zHl3E4EkEawTRCDAb0DoIY65dXInR4FBKeEMkGYwLQwQg10MFqINflwzIuV_1igNjvH6rEplyAv1XJpNFPDoCSi7_9Cb_NSElZnuWI4jkFo_kTduAlsTCG34vwhqT0bFA6WKvx3TU7_QeEaYY4-JwgR438I-FHgS661QLA48NmVO8uoPdhpj3ZatNPe22kVit49VLzsZhh_Sx79Q0AcgYpP6QbKU0v_SfsL_deocg</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2515476372</pqid></control><display><type>article</type><title>Cellular prion protein activates Caspase 3 for apoptotic defense mechanism in astrocytes</title><source>SpringerLink Journals</source><creator>Marques, Caroline M. S. ; Pedron, Tatiana ; Batista, Bruno L. ; Cerchiaro, Giselle</creator><creatorcontrib>Marques, Caroline M. S. ; Pedron, Tatiana ; Batista, Bruno L. ; Cerchiaro, Giselle</creatorcontrib><description>The cellular prion protein (PrP
C
) is anchored in the plasma membrane of cells, and it is highly present in cells of brain tissue, exerting numerous cellular and cognitive functions. The present study proves the importance of PrP
C
in the cellular defense mechanism and metal homeostasis in astrocytes cells. Through experimental studies using cell lines of immortalized mice astrocytes (wild type and knockout for PrP
C
), we showed that PrPc is involved in the apoptosis cell death process by the activation of Caspase 3, downregulation of p53, and cell cycle maintenance. Metal homeostasis was determined by inductively coupled plasma mass spectrometry technique, indicating the crucial role of PrP
C
to lower intracellular calcium. The lowered calcium concentration and the Caspase 3 downregulation in the PrP
C
-null astrocytes resulted in a faster growth rate in cells, comparing with PrP
C
wild-type one. The presence of PrP
C
shows to be essential to cell death and healthy growth. In conclusion, our results show for the first time that astrocyte knockout cells for the cellular prion protein could modulate apoptosis-dependent cell death pathways.
Graphic abstract</description><identifier>ISSN: 0300-8177</identifier><identifier>EISSN: 1573-4919</identifier><identifier>DOI: 10.1007/s11010-021-04078-5</identifier><identifier>PMID: 33547547</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Apoptosis ; Astrocytes ; Biochemistry ; Biomedical and Life Sciences ; Calcium ; Calcium (intracellular) ; Cardiology ; Caspase-3 ; Cell cycle ; Cell death ; Cell lines ; Cognitive ability ; Defense mechanisms ; Growth rate ; Homeostasis ; Inductively coupled plasma mass spectrometry ; Life Sciences ; Mass spectrometry ; Mass spectroscopy ; Medical Biochemistry ; Mortality ; Neurophysiology ; Oncology ; p53 Protein ; Prion protein ; Prions ; Proteins ; Tumor proteins</subject><ispartof>Molecular and cellular biochemistry, 2021-05, Vol.476 (5), p.2149-2158</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC part of Springer Nature 2021</rights><rights>COPYRIGHT 2021 Springer</rights><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC part of Springer Nature 2021.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c442t-a4c22b15aab3fe48319f368e7bee080a5c5d2a7d3efa5358f38f1738356068733</citedby><cites>FETCH-LOGICAL-c442t-a4c22b15aab3fe48319f368e7bee080a5c5d2a7d3efa5358f38f1738356068733</cites><orcidid>0000-0001-8606-5400</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11010-021-04078-5$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11010-021-04078-5$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51297</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33547547$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Marques, Caroline M. S.</creatorcontrib><creatorcontrib>Pedron, Tatiana</creatorcontrib><creatorcontrib>Batista, Bruno L.</creatorcontrib><creatorcontrib>Cerchiaro, Giselle</creatorcontrib><title>Cellular prion protein activates Caspase 3 for apoptotic defense mechanism in astrocytes</title><title>Molecular and cellular biochemistry</title><addtitle>Mol Cell Biochem</addtitle><addtitle>Mol Cell Biochem</addtitle><description>The cellular prion protein (PrP
C
) is anchored in the plasma membrane of cells, and it is highly present in cells of brain tissue, exerting numerous cellular and cognitive functions. The present study proves the importance of PrP
C
in the cellular defense mechanism and metal homeostasis in astrocytes cells. Through experimental studies using cell lines of immortalized mice astrocytes (wild type and knockout for PrP
C
), we showed that PrPc is involved in the apoptosis cell death process by the activation of Caspase 3, downregulation of p53, and cell cycle maintenance. Metal homeostasis was determined by inductively coupled plasma mass spectrometry technique, indicating the crucial role of PrP
C
to lower intracellular calcium. The lowered calcium concentration and the Caspase 3 downregulation in the PrP
C
-null astrocytes resulted in a faster growth rate in cells, comparing with PrP
C
wild-type one. The presence of PrP
C
shows to be essential to cell death and healthy growth. In conclusion, our results show for the first time that astrocyte knockout cells for the cellular prion protein could modulate apoptosis-dependent cell death pathways.
Graphic abstract</description><subject>Apoptosis</subject><subject>Astrocytes</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Calcium</subject><subject>Calcium (intracellular)</subject><subject>Cardiology</subject><subject>Caspase-3</subject><subject>Cell cycle</subject><subject>Cell death</subject><subject>Cell lines</subject><subject>Cognitive ability</subject><subject>Defense mechanisms</subject><subject>Growth rate</subject><subject>Homeostasis</subject><subject>Inductively coupled plasma mass spectrometry</subject><subject>Life Sciences</subject><subject>Mass spectrometry</subject><subject>Mass spectroscopy</subject><subject>Medical Biochemistry</subject><subject>Mortality</subject><subject>Neurophysiology</subject><subject>Oncology</subject><subject>p53 Protein</subject><subject>Prion protein</subject><subject>Prions</subject><subject>Proteins</subject><subject>Tumor proteins</subject><issn>0300-8177</issn><issn>1573-4919</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kd9rFDEQx4Mo9jz9B3yQBV982Zqfm9xjOdQKBV9a6FvIZSc1ZTc5k6zQ_965XmtRRBISmHy-k5n5EvKW0VNGqf5YGaOM9pSznkqqTa-ekRVTWvRywzbPyYoKSnvDtD4hr2q9pUhTxl6SEyGU1LhX5HoL07RMrnT7EnPCMzeIqXO-xZ-uQe22ru5dhU50IZfO7fO-5RZ9N0KAhPEZ_HeXYp27g6y2kv0d6l6TF8FNFd483Gty9fnT5fa8v_j25ev27KL3UvLWO-k53zHl3E4EkEawTRCDAb0DoIY65dXInR4FBKeEMkGYwLQwQg10MFqINflwzIuV_1igNjvH6rEplyAv1XJpNFPDoCSi7_9Cb_NSElZnuWI4jkFo_kTduAlsTCG34vwhqT0bFA6WKvx3TU7_QeEaYY4-JwgR438I-FHgS661QLA48NmVO8uoPdhpj3ZatNPe22kVit49VLzsZhh_Sx79Q0AcgYpP6QbKU0v_SfsL_deocg</recordid><startdate>20210501</startdate><enddate>20210501</enddate><creator>Marques, Caroline M. S.</creator><creator>Pedron, Tatiana</creator><creator>Batista, Bruno L.</creator><creator>Cerchiaro, Giselle</creator><general>Springer US</general><general>Springer</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QL</scope><scope>7QP</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-8606-5400</orcidid></search><sort><creationdate>20210501</creationdate><title>Cellular prion protein activates Caspase 3 for apoptotic defense mechanism in astrocytes</title><author>Marques, Caroline M. S. ; Pedron, Tatiana ; Batista, Bruno L. ; Cerchiaro, Giselle</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c442t-a4c22b15aab3fe48319f368e7bee080a5c5d2a7d3efa5358f38f1738356068733</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Apoptosis</topic><topic>Astrocytes</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Calcium</topic><topic>Calcium (intracellular)</topic><topic>Cardiology</topic><topic>Caspase-3</topic><topic>Cell cycle</topic><topic>Cell death</topic><topic>Cell lines</topic><topic>Cognitive ability</topic><topic>Defense mechanisms</topic><topic>Growth rate</topic><topic>Homeostasis</topic><topic>Inductively coupled plasma mass spectrometry</topic><topic>Life Sciences</topic><topic>Mass spectrometry</topic><topic>Mass spectroscopy</topic><topic>Medical Biochemistry</topic><topic>Mortality</topic><topic>Neurophysiology</topic><topic>Oncology</topic><topic>p53 Protein</topic><topic>Prion protein</topic><topic>Prions</topic><topic>Proteins</topic><topic>Tumor proteins</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Marques, Caroline M. S.</creatorcontrib><creatorcontrib>Pedron, Tatiana</creatorcontrib><creatorcontrib>Batista, Bruno L.</creatorcontrib><creatorcontrib>Cerchiaro, Giselle</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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 Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular and cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Marques, Caroline M. S.</au><au>Pedron, Tatiana</au><au>Batista, Bruno L.</au><au>Cerchiaro, Giselle</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cellular prion protein activates Caspase 3 for apoptotic defense mechanism in astrocytes</atitle><jtitle>Molecular and cellular biochemistry</jtitle><stitle>Mol Cell Biochem</stitle><addtitle>Mol Cell Biochem</addtitle><date>2021-05-01</date><risdate>2021</risdate><volume>476</volume><issue>5</issue><spage>2149</spage><epage>2158</epage><pages>2149-2158</pages><issn>0300-8177</issn><eissn>1573-4919</eissn><abstract>The cellular prion protein (PrP
C
) is anchored in the plasma membrane of cells, and it is highly present in cells of brain tissue, exerting numerous cellular and cognitive functions. The present study proves the importance of PrP
C
in the cellular defense mechanism and metal homeostasis in astrocytes cells. Through experimental studies using cell lines of immortalized mice astrocytes (wild type and knockout for PrP
C
), we showed that PrPc is involved in the apoptosis cell death process by the activation of Caspase 3, downregulation of p53, and cell cycle maintenance. Metal homeostasis was determined by inductively coupled plasma mass spectrometry technique, indicating the crucial role of PrP
C
to lower intracellular calcium. The lowered calcium concentration and the Caspase 3 downregulation in the PrP
C
-null astrocytes resulted in a faster growth rate in cells, comparing with PrP
C
wild-type one. The presence of PrP
C
shows to be essential to cell death and healthy growth. In conclusion, our results show for the first time that astrocyte knockout cells for the cellular prion protein could modulate apoptosis-dependent cell death pathways.
Graphic abstract</abstract><cop>New York</cop><pub>Springer US</pub><pmid>33547547</pmid><doi>10.1007/s11010-021-04078-5</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0001-8606-5400</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0300-8177 |
| ispartof | Molecular and cellular biochemistry, 2021-05, Vol.476 (5), p.2149-2158 |
| issn | 0300-8177 1573-4919 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2487156654 |
| source | SpringerLink Journals |
| subjects | Apoptosis Astrocytes Biochemistry Biomedical and Life Sciences Calcium Calcium (intracellular) Cardiology Caspase-3 Cell cycle Cell death Cell lines Cognitive ability Defense mechanisms Growth rate Homeostasis Inductively coupled plasma mass spectrometry Life Sciences Mass spectrometry Mass spectroscopy Medical Biochemistry Mortality Neurophysiology Oncology p53 Protein Prion protein Prions Proteins Tumor proteins |
| title | Cellular prion protein activates Caspase 3 for apoptotic defense mechanism in astrocytes |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-26T07%3A06%3A11IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Cellular%20prion%20protein%20activates%20Caspase%203%20for%20apoptotic%20defense%20mechanism%20in%20astrocytes&rft.jtitle=Molecular%20and%20cellular%20biochemistry&rft.au=Marques,%20Caroline%20M.%20S.&rft.date=2021-05-01&rft.volume=476&rft.issue=5&rft.spage=2149&rft.epage=2158&rft.pages=2149-2158&rft.issn=0300-8177&rft.eissn=1573-4919&rft_id=info:doi/10.1007/s11010-021-04078-5&rft_dat=%3Cgale_proqu%3EA659190587%3C/gale_proqu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2515476372&rft_id=info:pmid/33547547&rft_galeid=A659190587&rfr_iscdi=true |