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| Home > Publications Database > Mitochondria-Endoplasmic Reticulum Contact Sites Dynamics and Calcium Homeostasis Are Differentially Disrupted in PINK1-PD or PRKN-PD Neurons. > print |
| Home > Publications Database > Mitochondria-Endoplasmic Reticulum Contact Sites Dynamics and Calcium Homeostasis Are Differentially Disrupted in PINK1-PD or PRKN-PD Neurons. > print |
| 001 | 265796 | ||
| 005 | 20240112171450.0 | ||
| 024 | 7 | _ | |a 10.1002/mds.29525 |2 doi |
| 024 | 7 | _ | |a pmid:37449534 |2 pmid |
| 024 | 7 | _ | |a 0885-3185 |2 ISSN |
| 024 | 7 | _ | |a 1531-8257 |2 ISSN |
| 024 | 7 | _ | |a altmetric:151560259 |2 altmetric |
| 037 | _ | _ | |a DZNE-2023-01040 |
| 041 | _ | _ | |a English |
| 082 | _ | _ | |a 610 |
| 100 | 1 | _ | |a Grossmann, Dajana |0 0000-0002-2005-4546 |b 0 |
| 245 | _ | _ | |a Mitochondria-Endoplasmic Reticulum Contact Sites Dynamics and Calcium Homeostasis Are Differentially Disrupted in PINK1-PD or PRKN-PD Neurons. |
| 260 | _ | _ | |a New York, NY |c 2023 |b Wiley |
| 336 | 7 | _ | |a article |2 DRIVER |
| 336 | 7 | _ | |a Output Types/Journal article |2 DataCite |
| 336 | 7 | _ | |a Journal Article |b journal |m journal |0 PUB:(DE-HGF)16 |s 1700230864_11242 |2 PUB:(DE-HGF) |
| 336 | 7 | _ | |a ARTICLE |2 BibTeX |
| 336 | 7 | _ | |a JOURNAL_ARTICLE |2 ORCID |
| 336 | 7 | _ | |a Journal Article |0 0 |2 EndNote |
| 520 | _ | _ | |a It is generally believed that the pathogenesis of PINK1/parkin-related Parkinson's disease (PD) is due to a disturbance in mitochondrial quality control. However, recent studies have found that PINK1 and Parkin play a significant role in mitochondrial calcium homeostasis and are involved in the regulation of mitochondria-endoplasmic reticulum contact sites (MERCSs).The aim of our study was to perform an in-depth analysis of the role of MERCSs and impaired calcium homeostasis in PINK1/Parkin-linked PD.In our study, we used induced pluripotent stem cell-derived dopaminergic neurons from patients with PD with loss-of-function mutations in PINK1 or PRKN. We employed a split-GFP-based contact site sensor in combination with the calcium-sensitive dye Rhod-2 AM and applied Airyscan live-cell super-resolution microscopy to determine how MERCSs are involved in the regulation of mitochondrial calcium homeostasis.Our results showed that thapsigargin-induced calcium stress leads to an increase of the abundance of narrow MERCSs in wild-type neurons. Intriguingly, calcium levels at the MERCSs remained stable, whereas the increased net calcium influx resulted in elevated mitochondrial calcium levels. However, PINK1-PD or PRKN-PD neurons showed an increased abundance of MERCSs at baseline, accompanied by an inability to further increase MERCSs upon thapsigargin-induced calcium stress. Consequently, calcium distribution at MERCSs and within mitochondria was disrupted.Our results demonstrated how the endoplasmic reticulum and mitochondria work together to cope with calcium stress in wild-type neurons. In addition, our results suggests that PRKN deficiency affects the dynamics and composition of MERCSs differently from PINK1 deficiency, resulting in differentially affected calcium homeostasis. © 2023 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society. |
| 536 | _ | _ | |a 353 - Clinical and Health Care Research (POF4-353) |0 G:(DE-HGF)POF4-353 |c POF4-353 |f POF IV |x 0 |
| 588 | _ | _ | |a Dataset connected to CrossRef, PubMed, , Journals: pub.dzne.de |
| 650 | _ | 2 | |a Humans |2 MeSH |
| 650 | _ | 2 | |a Parkinson Disease: pathology |2 MeSH |
| 650 | _ | 2 | |a Calcium: metabolism |2 MeSH |
| 650 | _ | 2 | |a Thapsigargin: metabolism |2 MeSH |
| 650 | _ | 2 | |a Mitochondria: pathology |2 MeSH |
| 650 | _ | 2 | |a Dopaminergic Neurons: metabolism |2 MeSH |
| 650 | _ | 2 | |a Protein Kinases: genetics |2 MeSH |
| 650 | _ | 2 | |a Ubiquitin-Protein Ligases: genetics |2 MeSH |
| 650 | _ | 2 | |a Endoplasmic Reticulum: metabolism |2 MeSH |
| 650 | _ | 2 | |a Homeostasis |2 MeSH |
| 650 | _ | 7 | |a PTEN-induced putative kinase |0 EC 2.7.11.1 |2 NLM Chemicals |
| 650 | _ | 7 | |a PINK1 |2 Other |
| 650 | _ | 7 | |a Parkin |2 Other |
| 650 | _ | 7 | |a Parkinson's disease |2 Other |
| 650 | _ | 7 | |a calcium |2 Other |
| 650 | _ | 7 | |a mitochondria-ER contact sites |2 Other |
| 650 | _ | 7 | |a Calcium |0 SY7Q814VUP |2 NLM Chemicals |
| 650 | _ | 7 | |a Thapsigargin |0 67526-95-8 |2 NLM Chemicals |
| 650 | _ | 7 | |a Protein Kinases |0 EC 2.7.- |2 NLM Chemicals |
| 650 | _ | 7 | |a Ubiquitin-Protein Ligases |0 EC 2.3.2.27 |2 NLM Chemicals |
| 650 | _ | 7 | |a parkin protein |0 EC 2.3.2.27 |2 NLM Chemicals |
| 700 | 1 | _ | |a Malburg, Nina |b 1 |
| 700 | 1 | _ | |a Glaß, Hannes |0 0000-0003-3155-5300 |b 2 |
| 700 | 1 | _ | |a Weeren, Veronika |b 3 |
| 700 | 1 | _ | |a Sondermann, Verena |b 4 |
| 700 | 1 | _ | |a Pfeiffer, Julia F |b 5 |
| 700 | 1 | _ | |a Petters, Janine |b 6 |
| 700 | 1 | _ | |a Lukas, Jan |0 0000-0002-8061-5798 |b 7 |
| 700 | 1 | _ | |a Seibler, Philip |0 0000-0002-3496-7194 |b 8 |
| 700 | 1 | _ | |a Klein, Christine |0 0000-0003-2102-3431 |b 9 |
| 700 | 1 | _ | |a Grünewald, Anne |0 0000-0002-4179-2994 |b 10 |
| 700 | 1 | _ | |a Hermann, Andreas |0 P:(DE-2719)2811732 |b 11 |e Last author |
| 773 | _ | _ | |a 10.1002/mds.29525 |g Vol. 38, no. 10, p. 1822 - 1836 |0 PERI:(DE-600)2041249-6 |n 10 |p 1822 - 1836 |t Movement disorders |v 38 |y 2023 |x 0885-3185 |
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