Idiopathic Intracranial Hypertension and Multiple Sclerosis.

Unexplained elevated intracranial pressure occasionally develops in individuals with Multiple Sclerosis (MS). Visual symptoms and signs are common to both conditions. An awareness of this association is particularly relevant due to the increased incidence of headache in MS and the frequent overlap of symptoms and signs in both conditions.

Junb controls lymphatic vascular development in zebrafish via miR-182.

JUNB, a subunit of the AP-1 transcription factor complex, mediates gene regulation in response to a plethora of extracellular stimuli. Previously, JUNB was shown to act as a critical positive regulator of blood vessel development and homeostasis as well as a negative regulator of proliferation, inflammation and tumour growth. Here, we demonstrate that the oncogenic miR-182 is a novel JUNB target.

Epithelial deletion of podoplanin is dispensable for re-epithelialization of skin wounds.

The mucin-like transmembrane protein podoplanin (PDPN) is prominently represented in tumor-associated gene expression signatures of numerous types of cancer including squamous cell carcinoma, and gain-of-function and knockdown approaches in tissue culture strongly suggested an important role of PDPN in cell proliferation, migration and adhesion. PDPN is absent during epidermal homeostasis but is highly expressed in basal keratinocytes during cutaneous wound healing. Enhanced motility of immortalized keratinocytes upon ectopic PDPN overexpression argues for wound healing defects upon podoplanin deficiency in keratinocytes; however, in vivo data that unequivocally define the impact of PDPN by functional studies in a physiologically relevant system are still missing.

Collagenase-3 (MMP-13) deficiency protects C57BL/6 mice from antibody-induced arthritis.

Introduction: Matrix metalloproteinases (MMPs) are important in tissue remodelling. Here we investigate the role of collagenase-3 (MMP-13) in antibody-induced arthritis.

Methods: For this study we employed the K/BxN serum-induced arthritis model.