Apolipoprotein L genes are novel mediators of inflammation in beta cells

Paz-Barba, Miriam; Muñoz Garcia, Amadeo; de Winter, Twan J. J.; de Graaf, Natascha; van Agen, Maarten; van der Sar, Elisa; Lambregtse, Ferdy; Daleman, Lizanne; van der Slik, Arno; Zaldumbide, Arnaud; de Koning, Eelco J. P.; Carlotti, Françoise

doi:10.1007/s00125-023-06033-z

“…(19) APOL1 has shown to be upregulated in response to inflammation through the Janus kinase signal transducer and activator of transcription (JAK-STAT) pathway, a pathway also involved in the vitiligo pathogenesis. (20) Additionally, apolipoprotein E (APOE) was also reported to be downregulated in progressive as well as stable vitiligo patients compared to healthy controls, with the protein being more downregulated in stable vitiligo than the progressive form. Different sources imply that this protein has anti-inflammatory as well as pro-inflammatory properties.…”

Section: Resultsmentioning

confidence: 99%

Proteomics data in vitiligo: a scoping review

Berrevoet,

Van Nieuwerburgh,

Deforce

et al. 2024

Preprint

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An unbiased screening of which proteins are deregulated in vitiligo using proteomics can offer an enormous value. It could not only reveal robust biomarkers for detecting disease activity but can also identify which patients are most likely to respond to treatments. We performed a scoping review searching for all articles using proteomics in vitiligo. Eight manuscripts could be identified. Unfortunately, very limited overlap was found in the differentially expressed proteins between studies (15 out of 272; 5,51%) with variable degrees of the type of proteins and a substantial variety in the prevalence of acute phase proteins (range: 6-65%). Proteomics research has therefore brought little corroborating evidence on which proteins are differentially regulated between vitiligo patients and healthy controls or between active and stable vitiligo patients. While a limited patient size is an obvious weakness for several studies, an incomplete description of patient characteristics is an unfortunate and avoidable shortcoming. Additionally, the variations in the used methodology and analyses may further contribute to the overall observed variability. Nonetheless, more recent studies investigating the response to treatment seem to be more robust, as more differentially expressed proteins that have previously been confirmed to be involved in vitiligo were found. The further inclusion of proteomics analyses in clinical trials is recommended to increase insights into the pathogenic mechanisms in vitiligo and identify reliable biomarkers or promising drug targets. A harmonization in the study design, reporting and proteomics methodology could vastly improve the value of vitiligo proteomics research.

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“…PRDX6 has been reported as an activator of inflammatory pathways, as well as a protective mechanism by counteracting increased reactive oxygen species and repairing the membranes of oxidized cells caused by oxidative stress ( 21 ). APOL1 has shown to be upregulated in response to inflammation through the Janus kinase signal transducer and activator of transcription (JAK-STAT) pathway, a pathway also involved in the vitiligo pathogenesis ( 22 ). Additionally, apolipoprotein E (APOE) was also reported to be downregulated in progressive as well as stable vitiligo patients compared to healthy controls, with the protein being more downregulated in stable vitiligo than the progressive form.…”

Section: Resultsmentioning

confidence: 99%

Proteomics data in vitiligo: a scoping review

Berrevoet,

Van Nieuwerburgh,

Deforce

et al. 2024

Front. Immunol.

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An unbiased screening of which proteins are deregulated in vitiligo using proteomics can offer an enormous value. It could not only reveal robust biomarkers for detecting disease activity but can also identify which patients are most likely to respond to treatments. We performed a scoping review searching for all articles using proteomics in vitiligo. Eight manuscripts could be identified. Unfortunately, very limited overlap was found in the differentially expressed proteins between studies (15 out of 272; 5,51%) with variable degrees of the type of proteins and a substantial variety in the prevalence of acute phase proteins (range: 6-65%). Proteomics research has therefore brought little corroborating evidence on which proteins are differentially regulated between vitiligo patients and healthy controls or between active and stable vitiligo patients. While a limited patient size is an obvious weakness for several studies, an incomplete description of patient characteristics is an unfortunate and avoidable shortcoming. Additionally, the variations in the used methodology and analyses may further contribute to the overall observed variability. Nonetheless, more recent studies investigating the response to treatment seem to be more robust, as more differentially expressed proteins that have previously been confirmed to be involved in vitiligo were found. The further inclusion of proteomics analyses in clinical trials is recommended to increase insights into the pathogenic mechanisms in vitiligo and identify reliable biomarkers or promising drug targets. A harmonization in the study design, reporting and proteomics methodology could vastly improve the value of vitiligo proteomics research.

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“…To investigate the effect of inflammation of pancreatic cells, we explored part of a dataset we partially previously described earlier (( 16 ); GSE218316), to focus specifically on the two pro-inflammatory conditions (IL1β+IFNγ) and IFNα for the current study. This in vitro model and Wolfram-syndrome patient datasets were generated using the 10X-Genomics protocol.…”

Section: Methodsmentioning

confidence: 99%

Single-cell transcriptomics reveals a role for pancreatic duct cells as potential mediators of inflammation in diabetes mellitus

Muñoz García,

Juksar,

Groen

et al. 2024

Front. Immunol.

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IntroductionInflammation of the pancreas contributes to the development of diabetes mellitus. Although it is well-accepted that local inflammation leads to a progressive loss of functional beta cell mass that eventually causes the onset of the disease, the development of islet inflammation remains unclear.MethodsHere, we used single-cell RNA sequencing to explore the cell type-specific molecular response of primary human pancreatic cells exposed to an inflammatory environment.ResultsWe identified a duct subpopulation presenting a unique proinflammatory signature among all pancreatic cell types.DiscussionOverall, the findings of this study point towards a role for duct cells in the propagation of islet inflammation, and in immune cell recruitment and activation, which are key steps in the pathophysiology of diabetes mellitus.

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Apolipoprotein L genes are novel mediators of inflammation in beta cells

Cited by 5 publications

References 47 publications

Proteomics data in vitiligo: a scoping review

Proteomics data in vitiligo: a scoping review

Proteomics data in vitiligo: a scoping review

Single-cell transcriptomics reveals a role for pancreatic duct cells as potential mediators of inflammation in diabetes mellitus

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