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Myositis
Published in Jason Liebowitz, Philip Seo, David Hellmann, Michael Zeide, Clinical Innovation in Rheumatology, 2023
Simultaneously, with the detailed description of myopathological characteristics of patients with IMNM, two MSAs were detected that were present predominantly in patients with necrotizing myopathy: anti-signal recognition particle (anti-SRP) and anti-3-hydroxy-3-methylglutaryl-coA reductase (anti-HMGCR) antibodies. Anti-SRP antibodies were initially described in 1985,25 and these antibodies were seen in a subgroup of patients with severe necrotizing myopathy, rapidly progressive muscle weakness, highly elevated CPK, and frequent dysphagia.26–30 Patients develop muscle atrophy quite rapidly33 and can present with cardiac involvement.29, 34 The prevalence can range between 5 and 15%,30, 35 and women are affected more often than men.31, 32
Inflammatory Myopathy
Published in Maher Kurdi, Neuromuscular Pathology Made Easy, 2021
IMNM is a rare entity recently involved in the classification of IMs. It is characterized clinically with rapid disease course. The CK level is usually very high with 20–50 folds. Three autoantibodies have been shown to be associated with IMNM: anti-SRP, anti-HMGCoR, and anti-Jo1 antibodies. Anti-SRP has been explained before as a variant of PM that presents with severe necrotizing myopathy with absent or very minimal significant inflammation. It may be associated clinically with dysphagia, cardiomyopathy, and interstitial lung disease.
SRP72-Associated Bone Marrow Failure Syndrome
Published in Dongyou Liu, Handbook of Tumor Syndromes, 2020
SRP72 constitutes part of a ribonucleoprotein complex (signal recognition particle [SRP] complex, or signal recognition particle), which interacts with the ribosome (the other ribonucleoprotein particle) and targets secretory proteins to the rough ER, prior to integration into transmembrane or secreted proteins. Specifically, SRP72 and other SRP proteins (SRP9, SRP14, SRP19, SRP54, SRP68) bind the 7S RNA of ∼300 nt to form the SPR complex (either as monomers [SRP19 and SRP54] or heterodimers [SRP9/SRP14 and SRP68/SRP72]), which interacts directly with the docking protein in the ER membrane and mediates the transfer of integral membrane proteins and secretory proteins across the hydrophobic lipid bi-layers to the ER. The functionally independent Alu domain (SRP9/SRP14 and 5′/3′ ends of 7S RNA) in the SRP complex reaches into the factor binding site within the ribosomal 40S/60S subunit interface and is responsible for translation retardation (elongation arrest). The S domain (SRP19/SRP54/SRP68/SRP72) binds to the signal sequence emerging from the polypeptide exit tunnel in the signal pre-handover state. The multi-domain SRP GTPase SRP54 recognizes the signal with its M domain and establishes the targeting complex consisting of its NG domain bound to the homologous NG domain of the SRP receptor (SRαβ heterodimer) at the ER membrane in a GTP-dependent manner, which facilitates the targeting of ribosome bound nascent chain to the rough ER. Disassociation of the SRP complex from the ER allows resumption of elongation resumes and commencement of translocation [9,10].
The impact of chronic stress on the PFC transcriptome: a bioinformatic meta-analysis of publicly available RNA-sequencing datasets
Published in Stress, 2022
Using the same bioinformatic pipeline on each dataset revealed wide ranging effects on chronic stress on the PFC transcriptome. However, analysis of the combined datasets yielded 160 differentially expressed genes which suggests their general involvement in the response to chronic stress, regardless of paradigm specifics. Enrichment analysis of these genes revealed significant involvement in several processes including signal recognition particle (SRP)-co-translational targeting of proteins to membranes as well as ribosomal function. The SRP-pathway is initiated by the binding of SRP to a specific amino acid sequence on a nascent protein emerging from a translating ribosome. Translation is briefly halted while this complex is delivered to the plasma membrane via a cognate SRP receptor where it unloads the cargo. Translation resumes, SRP and SR dissociate and move on to other targets (Egea et al., 2005; Nagai et al., 2003; Saraogi & Shan, 2011). Combined with the findings that specific glutamatergic neurons are more affected than other cell types provide supporting evidence that chronic stress in the PFC disrupts excitatory neurotransmission and synaptic plasticity, going “off-line,” in part due to the dysregulated expression of membrane-bound proteins (Arnsten, 2009; Moghaddam, 2002).
Endothelial cell-derived extracellular vesicles alter vascular smooth muscle cell phenotype through high-mobility group box proteins
Published in Journal of Extracellular Vesicles, 2020
Michael J. Boyer, Yayoi Kimura, Tomoko Akiyama, Ariele Y. Baggett, Kyle J. Preston, Rosario Scalia, Satoru Eguchi, Victor Rizzo
To gain a broader view of the effects of EC-derived EV on VSMC phenotype, we performed unbiased mass spectroscopy analysis on VSMCs following incubation with the EVs derived from ECs. Using a cut-off for peptide fold-change at 1.5, we identified several peptides that were up-regulated in VSMC upon EC EV incubation (Figure 6, Online Figure X and Online Table VI). Gene ontology analysis and interactome analysis suggest that EC EVs induce VSMC proteins involved in metabolic regulations including those involved in mitochondrial respiration and response to stress. Of note, among these altered proteins were the pro-hypertrophy molecule, ribosomal protein S6, and pro-inflammatory molecules, HMGB1 and HMGB2 on the peptide level. On the protein level, 4 proteins (Srprb, Maoa, Rhot2 and Kdelr2) were up-regulated (Online Table VII). Signal recognition particle receptor β (Srprb) is necessary for sorting secretory and membrane proteins to the endoplasmic reticulum membranes, suggesting up-regulation of membrane protein synthesis and excretion [46].
Behavioural interventions that have the potential to improve self-care in adults with periodontitis: a systematic review
Published in Acta Odontologica Scandinavica, 2018
Mirkka Järvinen, Minna Stolt, Eino Honkala, Helena Leino-Kilpi, Marja Pöllänen
Since the clinical outcome measures that were used in the studies mainly described the state of oral hygiene (plaque indexes, plaque percent, bleeding indexes) and gingival inflammation, not the state or progression of periodontits, the variation in periodontitis definitions in the included studies doesn't seem to be a problem. Consistently, studies using behavioural methods or self-inspection showed significantly improved plaque control in the intervention group compared to control. Outcome measures such as probing pocket depth, x-rays and measurements of attachment loss would reveal the healing and recovery or progression of periodontitis. One included study reported PD measurements [33] as an outcome measure. Although this study showed a statistically significant reduction in the number of >4 mm pockets 3 months after treatment in the intervention group, this outcome should not be regarded solely as an effect of the behavioural approach. SRP was used in the beginning of the study, and patient self-care interventions were an additional but essential part of the treatment response. It is clear that periodontitis cannot be treated only by self-care. However, it can be concluded that behavioural interventions seem to improve the outcomes of self-care in periodontitis patients. Patients' skills, knowledge, level of motivation and values should therefore be taken into account in educational interventions for periodontitis patients.