Association between Caveolin-1 expression and pathophysiological progression of femoral nerves in diabetic foot amputation patients

Abstract Objective To evaluate the pathological changes of femoral nerves and the levels of caveolin-1 in diabetic foot amputation patients with neuropathy, and evaluate the association between caveolin-1 and neuropathy development. Method Thirty seven diabetic foot amputation patients were consecutively recruited from inpatients of Tianjin Metabolic Diseases Hospital between Jan 2003 and Nov 2005. Symptoms and signs of neuropathy, and scores of Toronto Clinical Scoring System (TCSS) were recorded. The nerve conduction velocity and HbA1c were measured. Femoral nerves were obtained 2-3 minutes after amputation. HE, Masson staining and transmission electron microscopy were used for pathological observation. Immunohistochemistry was used to observe changes of axons and count of nerve fiber density (NFD) and detect the levels of caveolin-1. Results HE, Masson and transmission electron microscopy showed nerve fibers were asymmetrical, the degenerated axons part had stronger staining and typical demyelinating changes. Stepwise regression models showed that HbA1c and NFD were the independent factors of caveolin-1 (F=45.090, p<0.001, R2=0.790) expression, and Caveolin-1, diabetes duration were independent factors of NFD (F=27.911, p<0.001, R2=0.691). Conclusion Caveolin-1 may be one of the key factors related to pathophysiological progression of femoral nerves in diabetic foot amputation patients.

[1]  R. Khan,et al.  Understanding Diabetic Foot Infection and its Management. , 2017, Diabetes & metabolic syndrome.

[2]  Dalong Zhu,et al.  Global epidemiology of diabetic foot ulceration: a systematic review and meta-analysis† , 2017, Annals of medicine.

[3]  Alessandro Bertuzzi,et al.  Insulin Signaling in Insulin Resistance States and Cancer: A Modeling Analysis , 2016, PloS one.

[4]  Jamal Ahmad,et al.  The diabetic foot. , 2016, Diabetes & metabolic syndrome.

[5]  Herbert F. Jelinek,et al.  Identifying Common Genetic Risk Factors of Diabetic Neuropathies , 2015, Front. Endocrinol..

[6]  L. Giurato,et al.  Management of negative pressure wound therapy in the treatment of diabetic foot ulcers. , 2015, World journal of orthopedics.

[7]  J. Nadler,et al.  Baicalein alleviates diabetic peripheral neuropathy through inhibition of oxidative–nitrosative stress and p38 MAPK activation , 2011, Experimental Neurology.

[8]  R. Dobrowsky,et al.  Caveolin-1 and Altered Neuregulin Signaling Contribute to the Pathophysiological Progression of Diabetic Peripheral Neuropathy , 2009, Diabetes.

[9]  F. Al-Mahroos,et al.  Diabetic neuropathy, foot ulceration, peripheral vascular disease and potential risk factors among patients with diabetes in bahrain: a nationwide primary care diabetes clinic-based study , 2007, Annals of Saudi medicine.

[10]  A. Boulton,et al.  Recent advances in the diagnosis and management of diabetic neuropathy. , 2005, The Journal of bone and joint surgery. British volume.

[11]  S. Kudoh,et al.  Diabetes mellitus may increase risk for idiopathic pulmonary fibrosis. , 2003, Chest.

[12]  E. Feldman,et al.  Caveolin‐1 expression in Schwann cells , 1999, Glia.

[13]  R. Medenica,et al.  [The diabetic foot]. , 1973, Revue medicale de la Suisse romande.

[14]  W. Freud Diabetes insipidus and pulmonary fibrosis. , 1955, A.M.A. archives of internal medicine.