Scientific Program

Conference Series Ltd invites all the participants across the globe to attend 8th International Conference of Orthopedic Surgeons and Rheumatology Rome, Italy.

Day 2 :

Keynote Forum

Giovanni Abatangelo

University of Padua, Italy

Keynote: Biological role of hyaluronic acid: possible involvement in pain control

Time : 09:45-10:25

OMICS International Rheumatology 2017 International Conference Keynote Speaker Giovanni Abatangelo photo
Biography:

Full Professor of Histology and Embriology, University of Padova, Italy. Graduated as MD (University of Padua, 1965), Postodctoral Specialization in Clinical Pathology (University of Padua, 1977), Postdoctoral Fellow Dept. of Biochemistry, Baylor University of Baylor, Houston, Texas, USA, (1965-1967), Lecturer, Institute of Histology, University of Padua (1970), Full Professor of Histology - Embryology, University of Padua (1975 - 2011) Senior Researcher of the Faculty of Medicine- University of Padova (2012- present) President of the Italian Society of Cutaneous Biology and Member of the Editorial Board of "Wound Repair and Regeneration" (Mosby Inc., St. Louis MO, USA).

Abstract:

Nociceptive pain is one of the most common types of pain and originates with an injury involving nociceptors. About 60% of the knee joint innervations are classified as nociceptive. The specific biological mechanism underlying the regulation of nociceptors is relevant for symptom treatment of pathologies affecting the knee joint. Indeed, intra-articular administration of exogenous hyaluronic acid (HA) in osteoarthritis (OA) seems to be particularly effective reducing pain and improving patient function. In the present work we investigated if HA induces activation of opioid peptide (OP) receptors.

Methods

In the present work we used both aequorin technology and the fluorescent dye Fura-2 to investigate if HA is able to induce putative antinociceptive effects via opioid receptor activation.

Results

Treatment with medium molecular weight (200 kDA) HA induces the selective activation of the kappa (KOP) receptor.

Keynote Forum

Yuxian Shen

Anhui Medical University, China

Keynote: The role of Mesencephalic Astrocyte-Derived Neurotrophic Factor (MANF) in inflammatory arthritis

Time : 10:25-11:05

OMICS International Rheumatology 2017 International Conference Keynote Speaker Yuxian Shen photo
Biography:

Yuxian Shen’s current research focused on the involvement of endoplasmic reticulum (ER) stress in the pathogenesises of neurodegenerative diseases and inflammatory diseases. The major findings in her lab are the results of protein degradation mediated by ER ubiquitin ligases of Hrd1 and gp78. Both of them facilitate degradation and enhance solubility of a-1-antitrypsin Z mutant, a major cause of a-1-antitrypsin deficiency. They also found that Hrd1 plays an important role in neuron protection. Additionally, Hrd1 promotes hyperphosphorylated tau degradation. An area of Shen’s lab is about ER stress-upregulated protein MANF. They found that MANF is sensitive to ischemia/hypoxia and inflammation. The results suggest that MANF may be involved in neuroprotection and inflammatory inhibition. Further efforts are directed to understand the transcription regulation of MANF under inflammation and ischemia. A new direction in her lab is to investigate the mechanisms of ER stress involved in autoimmune diseases including SLE and RA. 

Abstract:

Inflammation can cause endoplasmic reticulum (ER) stress and therefore activates the unfolded protein response (UPR). ER stress and the consequent UPR have the potential to activate NF-kB. However, the factors mediating the crosstalk between ER stress and the NF-κB pathway remain unclear. Here, we showed that ER stress inducible protein Mesencephalic Astrocyte-derived Neurotrophic Factor (MANF) was up-regulated in autoimmune diseases, such as rheumatoid arthritis, systemic lupus erythematosus, and ankylosing spondylitis, and inflammatory disease models. Inflammation caused MANF to relocalize to the nuclei. MANF interacted with the DNA binding domain of p65 through its C-terminal SAP-like domain in the nuclei under the condition of inflammation or ER stress. MANF consequently inhibited p65-mediated transcriptional activation by interfering with the binding of p65 to its target genes promoters. Consistently, MANF suppressed the expressions of NF-κB-dependent target genes and the proliferation of inflammatory synoviocytes. These findings suggest that MANF may be a negative regulator of inflammation and mediate the crosstalk between the NF-κB pathway and ER stress.