Abstract:
:Hereditary transthyretin amyloidosis (ATTR) is caused by amyloid deposition of misfolded transthyretin (TTR) in various tissues. Recently, reduction of circulating serum TTR, achieved via silencing oligonucleotides, was introduced as therapy of ATTR amyloidosis. We explored the impact of Serpin Family A Member 1 (SERPINA1) on TTR mRNA and protein expression. Oncostatin M (OSM) induced SERPINA1 in hepatoma cells and mice, while concomitantly TTR expression was significantly reduced. SERPINA1 knockdown resulted in specific elevated TTR expression in hepatoma cells; however other genes belonging to the group of acute phase proteins were unaffected. In mice, serum TTR was elevated after mSERPINA1 knockdown throughout antisense treatment. Following SERPINA1 knockdown, TTR deposition in several tissues, including dorsal root ganglia and intestine, was found to be increased, however numbers did not exceed significance levels. The data suggest that SERPINA1 is a co-factor of TTR expression. Our findings provide novel insight in the regulation of TTR and reveal a role of SERPINA1 in the pathogenesis of ATTR amyloidosis.
journal_name
Exp Cell Resjournal_title
Experimental cell researchauthors
Niemietz C,Bezerra F,Almeida MR,Guo S,Monia BP,Saraiva MJ,Schütz P,Schmidt HH,Zibert Adoi
10.1016/j.yexcr.2020.112217subject
Has Abstractpub_date
2020-10-15 00:00:00pages
112217issue
2eissn
0014-4827issn
1090-2422pii
S0014-4827(20)30466-3journal_volume
395pub_type
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