Topic
PDPN
About: PDPN is a research topic. Over the lifetime, 377 publications have been published within this topic receiving 11909 citations. The topic is also known as: T1A & Aggrus.
Papers published on a yearly basis
Papers
TL;DR: In this article, a cross-sectional descriptive study consisting of two phases was conducted to determine the prevalence of painful diabetic peripheral neuropathy (PDPN) in a population-based sample and to estimate its severity and impact.
Abstract: OBJECTIVE—To determine the prevalence of painful diabetic peripheral neuropathy (PDPN) in a population-based sample and to estimate its severity and impact.
RESEARCH DESIGN AND METHODS—A cross-sectional descriptive study consisting of two phases: phase 1, a postal survey to patients with type 2 diabetes (an initial screening questionnaire including one question about pain); phase 2, neurological history and examination using the Toronto Clinical Scoring System. Subjects with PDPN or mixed (PDPN and nonneuropathic) pain completed the Neuropathic Pain Scale and Neuroqol to assess severity and nature of the pain and impact on quality of life. Those without PDPN completed the Neuroqol only.
RESULTS—In phase 1, there was a 92.7% response (n = 326), with 208 (63.8%) subjects reporting pain. In phase 2, 269 (82.5%) subjects attended and 51 (19.0%) were found to have PDPN: 99 (36.8%) nonneuropathic pain, 20 (7.4%) mixed pain, and 99 (36.8%) no pain (PDPN prevalence 26.4%). Of those with PDPN, 80% stated that their pain was moderate or severe. Those affected had poorer quality of life than those with no pain (difference in mean scores 3.6 [95% CI 2.5–4.6%]) compared with those with nonneuropathic pain (1.7 [0.4–2.9%]). Both pain and neuropathy score were independently associated with quality of life, and subjects with PDPN had significantly higher neuropathy scores.
CONCLUSIONS—Our study showed a prevalence of PDPN of 26.4%. Having PDPN has a significant negative effect on quality of life, and increasing neuropathy is associated with an increasing risk of developing PDPN.
710 citations
TL;DR: Results indicate that podoplanin promotes tumor cell invasion in vitro and in vivo and induces collective cell migration by filopodia formation via the downregulation of the activities of small Rho family GTPases.
624 citations
TL;DR: It is suggested that CLEC-2 is a physiological target protein of podoplanin and imply that it is involved in podoplanIn-induced platelet aggregation, tumor metastasis, and other cellular responses related to podoplan in.
535 citations
TL;DR: It is demonstrated that platelets regulate lymphatic vascular development by directly interacting with lymphatic endothelial cells through C-type lectin-like receptor 2 (CLEC-2) receptors, identifying platelets as the cell type in which SLP-76 signaling is required to regulate lymphatics vascular development.
450 citations
TL;DR: It is found that human podoplanin directly interacts with ezrin (and moesin) in vitro and in vivo through a cluster of basic amino acids within its cytoplasmic tail, mainly through a juxtamembrane dipeptide RK.
Abstract: Podoplanin is a small membrane mucin expressed in tumors associated with malignant progression. It is enriched at cell-surface protrusions where it colocalizes with members of the ERM (ezrin, radixin, moesin) protein family. Here, we found that human podoplanin directly interacts with ezrin (and moesin) in vitro and in vivo through a cluster of basic amino acids within its cytoplasmic tail, mainly through a juxtamembrane dipeptide RK. Podoplanin induced an epithelial-mesenchymal transition in MDCK cells linked to the activation of RhoA and increased cell migration and invasiveness. Fluorescence time-lapse video observations in migrating cells indicate that podoplanin might be involved in ruffling activity as well as in retractive processes. By using mutant podoplanin constructs fused to green fluorescent protein we show that association of the cytoplasmic tail with ERM proteins is required for upregulation of RhoA activity and epithelial-mesenchymal transition. Furthermore, expression of either a dominant-negative truncated variant of ezrin or a dominant-negative mutant form of RhoA blocked podoplanin-induced RhoA activation and epithelial-mesenchymal transition. These results provide a mechanistic basis to understand the role of podoplanin in cell migration or invasiveness.
388 citations
Related Topics (5)
Performance Metrics
| Year | Papers |
|---|---|
| 2021 | 39 |
| 2020 | 48 |
| 2019 | 49 |
| 2018 | 42 |
| 2017 | 38 |
| 2016 | 35 |