scholarly journals Alpha-Fetoprotein Binding Mucin and Scavenger Receptors: An Available Bio-Target for Treating Cancer

2021 ◽  
Vol 11 ◽  
Author(s):  
Bo Lin ◽  
Qiujiao Wang ◽  
Kun Liu ◽  
Xu Dong ◽  
Mingyue Zhu ◽  
...  
Keyword(s):  
Drug Delivery ◽  
Signal Transduction ◽  
Immune Suppression ◽  
Theoretical Basis ◽  
Alpha Fetoprotein ◽  
Scavenger Receptors ◽  
Complex Carbohydrate ◽  
Targeting Therapy ◽  
Carbohydrate Polymer ◽  
Underlying Mechanisms

Alpha-fetoprotein (AFP) entrance into cancer cells is mediated by AFP receptors (AFPRs) and exerts malignant effects. Therefore, understanding the structure of AFPRs will facilitate the development of rational approaches for vaccine design, drug delivery, antagonizing immune suppression and diagnostic imaging to treat cancer effectively. Throughout the last three decades, the identification of universal receptors for AFP has failed due to their complex carbohydrate polymer structures. Here, we focused on the two types of binding proteins or receptors that may serve as AFPRs, namely, the A) mucin receptors family, and B) the scavenger family. We presented an informative review with detailed descriptions of the signal transduction, cross-talk, and interplay of various transcription factors which highlight the downstream events following AFP binding to mucin or scavenger receptors. We mainly explored the underlying mechanisms involved mucin or scavenger receptors that interact with AFP, provide more evidence to support these receptors as tumor AFPRs, and establish a theoretical basis for targeting therapy of cancer.

Microenvironment Responsive DNA-conjugated Albumin Nanocarriers for Targeting Therapy

2021 ◽  
Author(s):  
Jiayu Yu ◽  
Jianing Zhang ◽  
Jing Jin ◽  
Wei Jiang
Keyword(s):  
Drug Delivery ◽  
Cancer Therapy ◽  
Bovine Serum Albumin ◽  
Serum Albumin ◽  
Bovine Serum ◽  
Efficient Treatment ◽  
Targeting Therapy

Drug delivery with accurate targeting and efficient treatment has become an essential strategy for cancer therapy. Two nanocarriers based on bovine serum albumin (BSA) and DNA were synthesized by click...

scholarly journals Melatonin Improves Glucose Homeostasis and Endothelial Vascular Function in High-Fat Diet-Fed Insulin-Resistant Mice

Endocrinology ◽  
2009 ◽  
Vol 150 (12) ◽  
pp. 5311-5317 ◽  
Author(s):  
Claudio Sartori ◽  
Pierre Dessen ◽  
Caroline Mathieu ◽  
Anita Monney ◽  
Jonathan Bloch ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Signal Transduction ◽  
Glucose Tolerance ◽  
Glucose Homeostasis ◽  
High Fat Diet ◽  
High Fat ◽  
Insulin Resistant ◽  
Normal Chow ◽  
Underlying Mechanisms

Abstract Obesity and insulin resistance represent a problem of utmost clinical significance worldwide. Insulin-resistant states are characterized by the inability of insulin to induce proper signal transduction leading to defective glucose uptake in skeletal muscle tissue and impaired insulin-induced vasodilation. In various pathophysiological models, melatonin interacts with crucial molecules of the insulin signaling pathway, but its effects on glucose homeostasis are not known. In a diet-induced mouse model of insulin resistance and normal chow-fed control mice, we sought to assess the effects of an 8-wk oral treatment with melatonin on insulin and glucose tolerance and to understand underlying mechanisms. In high-fat diet-fed mice, but not in normal chow-fed control mice, melatonin significantly improved insulin sensitivity and glucose tolerance, as evidenced by a higher rate of glucose infusion to maintain euglycemia during hyperinsulinemic clamp studies and an attenuated hyperglycemic response to an ip glucose challenge. Regarding underlying mechanisms, we found that melatonin restored insulin-induced vasodilation to skeletal muscle, a major site of glucose utilization. This was due, at least in part, to the improvement of insulin signal transduction in the vasculature, as evidenced by increased insulin-induced phosphorylation of Akt and endoethelial nitric oxide synthase in aortas harvested from melatonin-treated high-fat diet-fed mice. In contrast, melatonin had no effect on the ability of insulin to promote glucose uptake in skeletal muscle tissue in vitro. These data demonstrate for the first time that in a diet-induced rodent model of insulin resistance, melatonin improves glucose homeostasis by restoring the vascular action of insulin.

scholarly journals 5-ASA-loaded SiO2 nanoparticles-a novel drug delivery system targeting therapy on ulcerative colitis in mice

2017 ◽  
Vol 15 (3) ◽  
pp. 1117-1122 ◽  
Author(s):  
Haiying Tang ◽  
Dan Xiang ◽  
Feng Wang ◽  
Jingwei Mao ◽  
Xiaoyan Tan ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Drug Delivery ◽  
Drug Delivery System ◽  
Delivery System ◽  
Sio2 Nanoparticles ◽  
Targeting Therapy ◽  
Novel Drug Delivery System ◽  
Novel Drug

scholarly journals Maternal nutrition and the developmental origins of osteoporosis in offspring: Potential mechanisms and clinical implications

2018 ◽  
Vol 243 (10) ◽  
pp. 836-842 ◽  
Author(s):  
Jia Zheng ◽  
Qianyun Feng ◽  
Sheng Zheng ◽  
Xinhua Xiao
Keyword(s):  
Early Life ◽  
Theoretical Basis ◽  
Complex Disease ◽  
Maternal Nutrition ◽  
Developmental Origins ◽  
Early Prevention ◽  
Environment Exposure ◽  
Prevention Of Osteoporosis ◽  
Health And Disease ◽  
Underlying Mechanisms

Osteoporosis, the most frequent metabolic disorder of bone, is a complex disease with a multifactorial origin that is influenced by genes and environments. However, the pathogenesis of osteoporosis has not been fully elucidated. The theory of “Developmental Origins of Health and Disease” indicates that early life environment exposure determines the risks of cardiometabolic diseases in adulthood. However, investigations into the effects of maternal nutrition and nutrition exposure during early life on the development of osteoporosis are limited. Recently, emerging evidence has strongly suggested that maternal nutrition has long-term influences on bone metabolism in offspring, and epigenetic modifications maybe the underlying mechanisms of this process. This review aimed to address maternal nutrition and its implications for the developmental origins of osteoporosis in offspring. It is novel in providing a theoretical basis for the early prevention of osteoporosis. Impact statement Our review aimed to address maternal nutrition and its implications for the developmental origins of osteoporosis in offspring, that can novelly provide a theoretical basis for the early prevention of osteoporosis.

Biofunctionalized dendritic polyaniline nanofiber for in situ amplified glucometer-based enzyme immunoassay of tumor marker

2015 ◽  
Vol 7 (5) ◽  
pp. 1843-1848 ◽  
Author(s):  
Sheng Wu ◽  
Jinsuo Chen ◽  
Yujian Tian ◽  
Xiaoming Tang ◽  
Wei Li ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Tumor Marker ◽  
Enzyme Immunoassay ◽  
Alpha Fetoprotein ◽  
Sensitive Detection ◽  
Polyaniline Nanofibers ◽  
Polyaniline Nanofiber

A new glucometer-based enzyme immunoassay was developed for the sensitive detection of alpha-fetoprotein using biofunctional dendritic polyaniline nanofibers as the signal-transduction tag.

scholarly journals Intracellular elevations of free calcium induced by activation of histamine H1 receptors in interphase and mitotic HeLa cells: hormone signal transduction is altered during mitosis.

1988 ◽  
Vol 107 (6) ◽  
pp. 2533-2539 ◽  
Author(s):  
M Volpi ◽  
R D Berlin
Keyword(s):  
Signal Transduction ◽  
Intracellular Calcium ◽  
Hela Cells ◽  
Calcium Influx ◽  
Tumor Promoter ◽  
Free Calcium ◽  
Interphase Cells ◽  
Underlying Mechanisms ◽  
Histamine H1 Receptors ◽  
Transient Elevation

A broad range of membrane functions, including endocytosis and exocytosis, are strongly inhibited during mitosis. The underlying mechanisms are unclear, however, but will probably be important in relation to the mitotic cycle and the regulation of surface phenomena generally. A major unanswered question is whether membrane signal transduction is altered during mitosis; suppression of an intracellular calcium [( Ca2+]i) transient could inhibit exocytosis; [Ca2+]i elevation could disassemble the mitotic spindle. Activation of the histamine H1 receptor interphase in HeLa cells is shown here by Indo-1 fluorescence to produce a transient elevation of [Ca2+]i. The [Ca2+]i transient consists of an initial sharp rise that is at least partially dependent on intracellular calcium followed by an elevated plateau that is absolutely dependent on extracellular calcium. The [Ca2+]i transient is completely suppressed by preincubation with the tumor promoter, phorbol myristate acetate, but is unaffected by preincubation with pertussis toxin (islet-activating protein). In mitotic (metaphase-arrested) HeLa cells, the [Ca2+]i transient is largely limited to the initial peak. Measurement of 45Ca2+ uptake shows that it is stimulated by histamine in interphase cells, but not in mitotics. We conclude that the histamine-stimulated generation of the second messenger, [Ca2+]i, in mitotic cells is limited by failure to activate a sustained calcium influx. The initial phase of calcium mobilization from intracellular stores is comparable to that in interphase cells. Hormone signal transduction thus appears to be altered during mitosis.

scholarly journals Regulation of Hedgehog Signal Transduction by Ubiquitination and Deubiquitination

2021 ◽  
Vol 22 (24) ◽  
pp. 13338
Author(s):  
Qing Zhang ◽  
Jin Jiang
Keyword(s):  
Signal Transduction ◽  
Transmembrane Protein ◽  
Cubitus Interruptus ◽  
Congenital Diseases ◽  
Gli Proteins ◽  
Family Protein ◽  
Wide Range ◽  
Human Disorders ◽  
Underlying Mechanisms ◽  
Hedgehog Signal

The Hedgehog (Hh) family of secreted proteins governs embryonic development and adult tissue homeostasis in species ranging from insects to mammals. Deregulation of Hh pathway activity has been implicated in a wide range of human disorders, including congenital diseases and cancer. Hh exerts its biological influence through a conserved signaling pathway. Binding of Hh to its receptor Patched (Ptc), a twelve-span transmembrane protein, leads to activation of an atypical GPCR family protein and Hh signal transducer Smoothened (Smo), which then signals downstream to activate the latent Cubitus interruptus (Ci)/Gli family of transcription factors. Hh signal transduction is regulated by ubiquitination and deubiquitination at multiple steps along the pathway including regulation of Ptc, Smo and Ci/Gli proteins. Here we review the effect of ubiquitination and deubiquitination on the function of individual Hh pathway components, the E3 ubiquitin ligases and deubiquitinases involved, how ubiquitination and deubiquitination are regulated, and whether the underlying mechanisms are conserved from Drosophila to mammals.

scholarly journals Biocompatible Nanocarriers for Enhanced Cancer Photodynamic Therapy Applications

Pharmaceutics ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 1933
Author(s):  
Sathish Sundar Dhilip Kumar ◽  
Heidi Abrahamse
Keyword(s):  
Drug Delivery ◽  
Photodynamic Therapy ◽  
Cancer Treatment ◽  
Targeting Therapy ◽  
Potential Applications ◽  
Carrier Molecule ◽  
Novel Material ◽  
Potential Benefits ◽  
Targeted Photodynamic Therapy

In recent years, the role of nanotechnology in drug delivery has become increasingly important, and this field of research holds many potential benefits for cancer treatment, particularly, in achieving cancer cell targeting and reducing the side effects of anticancer drugs. Biocompatible and biodegradable properties have been essential for using a novel material as a carrier molecule in drug delivery applications. Biocompatible nanocarriers are easy to synthesize, and their surface chemistry often enables them to load different types of photosensitizers (PS) to use targeted photodynamic therapy (PDT) for cancer treatment. This review article explores recent studies on the use of different biocompatible nanocarriers, their potential applications in PDT, including PS-loaded biocompatible nanocarriers, and the effective targeting therapy of PS-loaded biocompatible nanocarriers in PDT for cancer treatment. Furthermore, the review briefly recaps the global clinical trials of PDT and its applications in cancer treatment.

scholarly journals Advanced glycation end-products regulate extracellular matrix-adipocyte metabolic crosstalk in diabetes

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Clarissa Strieder-Barboza ◽  
Nicki A. Baker ◽  
Carmen G. Flesher ◽  
Monita Karmakar ◽  
Christopher K. Neeley ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Adipose Tissue ◽  
Glucose Uptake ◽  
Rho Gtpases ◽  
Cell Types ◽  
Scavenger Receptors ◽  
Advanced Glycation ◽  
Human Diabetes ◽  
Multiple Cell ◽  
Underlying Mechanisms

AbstractThe adipose tissue extracellular matrix (ECM) regulates adipocyte cellular metabolism and is altered in obesity and type 2 diabetes, but mechanisms underlying ECM-adipocyte metabolic crosstalk are poorly defined. Advanced glycation end-product (AGE) formation is increased in diabetes. AGE alter tissue function via direct effects on ECM and by binding scavenger receptors on multiple cell types and signaling through Rho GTPases. Our goal was to determine the role and underlying mechanisms of AGE in regulating human ECM-adipocyte metabolic crosstalk. Visceral adipocytes from diabetic and non-diabetic humans with obesity were studied in 2D and 3D-ECM culture systems. AGE is increased in adipose tissue from diabetic compared to non-diabetic subjects. Glycated collagen 1 and AGE-modified ECM regulate adipocyte glucose uptake and expression of AGE scavenger receptors and Rho signaling mediators, including the DIAPH1 gene, which encodes the human Diaphanous 1 protein (hDia1). Notably, inhibition of hDia1, but not scavenger receptors RAGE or CD36, attenuated AGE-ECM inhibition of adipocyte glucose uptake. These data demonstrate that AGE-modification of ECM contributes to adipocyte insulin resistance in human diabetes, and implicate hDia1 as a potential mediator of AGE-ECM-adipocyte metabolic crosstalk.

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