Mesenchymal stem cell treatment for peripheral nerve injury: a narrative review.

Peripheral nerve injuries occur as the result of sudden trauma and lead to reduced quality of life. The peripheral nervous system has an inherent capability to regenerate axons. However, peripheral nerve regeneration following injury is generally slow and incomplete that results in poor functional outcomes such as muscle atrophy. Although conventional surgical procedures for peripheral nerve injuries present many benefits, there are still several limitations including scarring, difficult accessibility to donor nerve, neuroma formation and a need to sacrifice the autologous nerve. For many years, other therapeutic approaches for peripheral nerve injuries have been explored, the most notable being the replacement of Schwann cells, the glial cells responsible for clearing out debris from the site of injury. Introducing cultured Schwann cells to the injured sites showed great benefits in promoting axonal regeneration and functional recovery. However, there are limited sources of Schwann cells for extraction and difficulties in culturing Schwann cells in vitro. Therefore, novel therapeutic avenues that offer maximum benefits for the treatment of peripheral nerve injuries should be investigated. This review focused on strategies using mesenchymal stem cells to promote peripheral nerve regeneration including exosomes of mesenchymal stem cells, nerve engineering using the nerve guidance conduits containing mesenchymal stem cells, and genetically engineered mesenchymal stem cells. We present the current progress of mesenchymal stem cell treatment of peripheral nerve injuries.

Complex effects of apoplexy secondary to pituitary adenoma.

Pituitary adenoma apoplexy is a well-known clinical syndrome induced by insulin infusion, cardiac surgery, trauma, and hypothalamic releasing factors. Pituitary apoplexy can cause secondary cerebral infarct and internal carotid artery occlusion. With blockade of tumor perfusion, apoplexy triggers a sudden onset of headache, visual impairment, cranial nerve palsy, disturbances of consciousness, eyelid ptosis, and hemiparesis. However, pituitary adenoma cells with high metabolic demand cannot survive with deficient blood supply and glucose concentrations. Moreover, a number of case reports have shown that spontaneous remission of syndromes, such as acromegaly, may be caused by pituitary adenoma after apoplexy. Therefore, understanding mechanism that underlies the balance between pituitary adenoma apoplexy and subsequent spontaneous remission of syndromes may suggest new approaches for treatment of pituitary adenoma apoplexy.

[Yeast-based production, purification and bioactivity assay of rainbow trout LECT2].

Leukocyte cell-derived chemotaxin 2 (LECT2) is a secretory cytokine that functions in many physiological and pathological processes. We used a Pichia pastoris expression system for the recombinant expression of rainbow trout LECT2. The recombinant LECT2 was purified by UNOsphere S Cation exchange and size-exclusion chromatography columns. The obtained target protein was highly pure (>96% homogeneity) and the yield was >120 mg/L of yeast cultures. An in vitro chamber assay revealed that recombinant LECT2 could induce chemotactic responses in rainbow trout head kidney-derived macrophages. Recombinant LECT2 not only enhanced macrophage respiratory burst activity and bactericidal activity, but also changed macrophage gene expression. In summary, we established a rapid and efficient method to prepare active recombinant rainbow trout LECT2 using a yeast expression system and column chromatography. Bioactive recombinant LECT2 is essential for studies on protein functions.

LECT2 protects mice against bacterial sepsis by activating macrophages via the CD209a receptor.

Leukocyte cell-derived chemotaxin 2 (LECT2) is a multifunctional cytokine and reduced plasma levels were found in patients with sepsis. However, precise functions and mechanisms of LECT2 remain unclear. The aim of the present study was to determine the role of LECT2 in modulating immune responses using mouse sepsis models. We found that LECT2 treatment improved outcome in mice with bacterial sepsis. Macrophages (MΦ), but not polymorphonuclear neutrophils, mediated the beneficial effect of LECT2 on bacterial sepsis. LECT2 treatment could alter gene expression and enhance phagocytosis and bacterial killing of MΦ in vitro. CD209a was identified to specifically interact with LECT2 and mediate LECT2-induced MΦ activation. CD209a-expressing MΦ was further confirmed to mediate the effect of LECT2 on sepsis in vivo. Our data demonstrate that LECT2 improves protective immunity in bacterial sepsis, possibly as a result of enhanced MΦ functions via the CD209a receptor. The modulation of MΦ functions by LECT2 may serve as a novel potential treatment for sepsis.

[Expression and significance of ß adrenergic receptors in a model of left ventricular mechanical unloading].

OBJECTIVE: To study the expression and significance of ß adrenergic receptors mRNA in a model of left ventricular mechanical unloading, and explore the change in cardiomyocyte in molecular level after left ventricular unloading. METHODS: Heart failure was reproduced in Lewis rats by ligating left anterior descending (LAD) artery. After 4 weeks, the failing hearts and right lungs were heterotopically transplanted into the abdomen of the recipients by anastomosing their ascending aorta to the recipients' descending aorta in the heart transplantation group. Two weeks after transplantation, heart weight, left ventricular weight, myocyte diameter and myocardial fibrosis were determined , and ß adrenergics receptors mRNA expression was essayed by real-time polymerase chain reaction (PCR). Seven normal Lewis rats served as control. RESULTS: The weight of the enlarged heart, left ventricular weight and myocyte diameter of the failing hearts were decreased to normal after transplantation. The levels of ß1- and ß2- adrenergic receptors mRNA expression were significantly lowered in heart failure group compared with that of normal group(0.09 ± 0.03 vs. 0.18 ± 0.04, 0.07 ± 0.06 vs. 0.12 ± 0.02, both P <0.05). The level of ß2- adrenergic receptor mRNA expression in heart transplantation group (0.11 ± 0.05) rose to normal (P>0.05), but ß1- adrenergic receptor mRNA expression (0.08 ± 0.06) was lower in heart transplantation group than that in normal group (P<0.05). CONCLUSION: Myocardium reverse remodeling after left ventricular unloading is accompanied by the change in cardiomyocyte in molecular level , such as the change in ß adrenergic receptors , which may involve in the improvement of heart function after being supported by left ventricular assist device.