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Serum Proteome Alterations in Human Cystathionine β-Synthase Deficiency and Ischemic Stroke Subtypes. | LitMetric

AI Article Synopsis

  • Ischemic stroke leads to brain damage through blood clotting processes, and cystathionine β-synthase deficiency (CBS) increases the risk of such events due to its role in vascular issues.
  • A study compared serum proteins in CBS-deficient patients and various types of ischemic stroke patients, using mass spectrometry to identify differences in protein expression.
  • The results showed overlaps in protein changes between CBS deficiency and ischemic stroke, especially within the cardioembolic subtype, indicating possible shared molecular mechanisms influencing both conditions.

Article Abstract

Ischemic stroke induces brain injury via thrombotic or embolic mechanisms involving large or small vessels. Cystathionine β-synthase deficiency (CBS), an inborn error of metabolism, is associated with vascular thromboembolism, the major cause of morbidity and mortality in affected patients. Because thromboembolism involves the brain vasculature in these patients, we hypothesize that CBS deficiency and ischemic stroke have similar molecular phenotypes. We used label-free mass spectrometry for quantification of changes in serum proteomes in CBS-deficient patients ( = 10) and gender/age-matched unaffected controls ( = 14), as well as in patients with cardioembolic ( = 17), large-vessel ( = 26), or lacunar ( = 25) ischemic stroke subtype. In CBS-deficient patients, 40 differentially expressed serum proteins were identified, of which 18 were associated with elevated homocysteine (Hcy) and 22 were Hcy-independent. We also identified Hcy-independent differentially expressed serum proteins in ischemic stroke patients, some of which were unique to a specific subtype: 10 of 32 for cardioembolic vs. large-vessel, six of 33 for cardioembolic vs. lacunar, and six of 23 for large-vessel vs. lacunar. There were significant overlaps between proteins affected by CBS deficiency and ischemic stroke, particularly the cardioembolic subtype, similar to protein overlaps between ischemic stroke subtypes. Top molecular pathways affected by CBS deficiency and ischemic stroke subtypes included acute phase response signaling and coagulation system. Similar molecular networks centering on NFκB were affected by CBS deficiency and stroke subtypes. These findings suggest common mechanisms involved in the pathologies of CBS deficiency and ischemic stroke subtypes.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6627068PMC
http://dx.doi.org/10.3390/ijms20123096DOI Listing

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