Evidence that muscle cells do not express the histidine-rich glycoprotein associated with AMP deaminase but can internalise the plasma protein

Histidine-rich glycoprotein (HRG) is synthesized by liver and is present at relatively high concentration in the plasma of vertebrates. We have previously described the association of a HRG-like molecule to purified rabbit skeletal muscle AMP deaminase (AMPD). We also provided the first evidence for the presence of a HRG-like protein in human skeletal muscle where a positive correlation between HRG content and total determined AMPD activity has been shown. In the present paper we investigate the origin of skeletal muscle HRG. The screening of a human skeletal muscle cDNA expression library using an anti-HRG antibody failed to reveal any positive clone. The RT-PCR analysis, performed on human skeletal muscle RNA as well as on RNA from the rhabdomyosarcoma (RD) cell line, failed to show any mRNA specific for the plasma HRG or for the putative muscle variant. When the RD cells were incubated with human plasma HRG, a time-dependent increase of the HRG immunoreactivity was detected both at the plasma membrane level and intracellularly. The internalisation of HRG was inhibited by the addition of heparin. The above data strongly suggest that skeletal muscle cells do not synthesize the muscle variant of HRG but instead can actively internalise it from plasma

Salivary Expression of S100A7/Psoriasin and Oral Damage in Primary Sjögren's Syndrome and Overlapping Disorders.

S100A7/psoriasin, a protein belonging to the S100A family of Ca2+ binding proteins, is known to exhibit an antimicrobial activity but it has also been implicated in the regulation of cell proliferation, differentiation, invasion and metastasis. By using a proteomic approach, S100A7/psoriasin has been recently identified in the whole saliva of patients with Systemic Sclerosis as a potential disease biomarker. The aim of the present study were : 1) to compare the expression of salivary S100A7/psoriasin in patients with Sjogren's Syndrome associated to anti-centromere antibodies (ACA) positive Systemic Sclerosis (SS-SSc) versus patients with primary Sjogren's Syndrome (pSS) and 2) to explore any correlation between salivary S100A7/psoriasin and oral damage. S100A7/psoriasin levels were significantly higher in SS-SSc subjects; S100A7/psoriasin salivary levels negatively correlated with the unstimulated salivary flow (USF) rate; The salivary expression of the protein was significantly associated with the Sjogren's Syndrome disease damage index and specifically with the complete loss of teeth. In conclusion, salivary S100A7/psoriasin might be useful in differentiating pSS from SS-SSc and seems to be able to reflect oral damage in both pSS and SS overlapping disorders