Lysosome-Targeting Strategy Using Polypeptides and Chimeric Molecules

: Hyaluronan (HA) is a natural linear polysaccharide that has excellent hydrophilicity, biocompatibility, biodegradability, and low immunogenicity, making it one of the most attractive biopolymers used for biomedical researches and applications. Due to the multiple functional sites on HA and its intrinsic affinity for CD44, a receptor highly expressed on various cancer cells, HA has been widely engineered to construct different drug-loading nanoparticles (NPs) for CD44- targeted anti-tumor therapy. When a cocktail of drugs is co-loaded in HA NP, a multifunctional nano-carriers could be obtained, which features as a highly effective and self-targeting strategy to combat the cancers with CD44 overexpression. The HA-based multidrug nano-carriers can be a combination of different drugs, various therapeutic modalities, or the integration of therapy and diagnostics (theranostics). Up to now, there are many types of HA-based multidrug nano-carriers constructed by different formulation strategies including drug co-conjugates, micelles, nano-gels and hybrid NP of HA and so on. This multidrug nano-carrier takes the full advantages of HA as NP matrix, drug carriers and targeting ligand, representing a simplified and biocompatible platform to realize the targeted and synergistic combination therapy against the cancers. In this review, recent progresses about HA-based multidrug nano-carriers for combination cancer therapy are summarized and its potential challenges for translational applications have been discussed.

Automated Oxygen Saturation Targeting Strategy in Neonates

The Journal of Pediatrics ◽

10.1016/j.jpeds.2021.04.055 ◽

2021 ◽

Author(s):

Jogender Kumar ◽

Jitendra Meena

Keyword(s):

Oxygen Saturation ◽

Targeting Strategy

Optimal Low-Thrust Earth-Moon Targeting Strategy for N-Body Problem

Journal of Guidance Control and Dynamics ◽

10.2514/2.4755 ◽

2001 ◽

Vol 24 (3) ◽

pp. 626-628 ◽

Cited By ~ 1

Author(s):

Hui Yan ◽

Hongxin Wu

Keyword(s):

Body Problem ◽

Low Thrust ◽

N Body Problem ◽

Targeting Strategy

Generation ofLeishmaniamutants lacking antibiotic resistance genes using a versatile hit-and-run targeting strategy

FEMS Microbiology Letters ◽

10.1111/j.1574-6968.2004.tb09571.x ◽

2004 ◽

Vol 235 (1) ◽

pp. 89-94 ◽

Cited By ~ 10

Author(s):

Hubert Denise ◽

Graham H. Coombs ◽

Jeremy C. Mottram

Keyword(s):

Antibiotic Resistance ◽

Resistance Genes ◽

Antibiotic Resistance Genes ◽

Hit And Run ◽

Targeting Strategy

Light-controlled endosomal escape of the novel CD133-targeting immunotoxin AC133–saporin by photochemical internalization — A minimally invasive cancer stem cell-targeting strategy

Journal of Controlled Release ◽

10.1016/j.jconrel.2015.03.008 ◽

2015 ◽

Vol 206 ◽

pp. 37-48 ◽

Cited By ~ 42

Author(s):

Monica Bostad ◽

Cathrine Elisabeth Olsen ◽

Qian Peng ◽

Kristian Berg ◽

Anders Høgset ◽

...

Keyword(s):

Stem Cell ◽

Minimally Invasive ◽

Cancer Stem Cell ◽

Invasive Cancer ◽

Endosomal Escape ◽

The Novel ◽

Cell Targeting ◽

Photochemical Internalization ◽

Targeting Strategy

Surface-engineered dendrimers for dual drug delivery: A receptor up-regulation and enhanced cancer targeting strategy

Journal of Drug Targeting ◽

10.1080/10611860802473154 ◽

2008 ◽

Vol 16 (10) ◽

pp. 758-772 ◽

Cited By ~ 77

Author(s):

Rakesh Kumar Tekade ◽

Tathagata Dutta ◽

Abhishek Tyagi ◽

Alok Chandra Bharti ◽

Bhudev Chandra Das ◽

...

Keyword(s):

Drug Delivery ◽

Cancer Targeting ◽

Targeting Strategy ◽

Dual Drug

The frequency of chimeric molecules as a consequence of PCR co-amplification of 16S rRNA genes from different bacterial species

Microbiology ◽

10.1099/13500872-142-5-1107 ◽

1996 ◽

Vol 142 (5) ◽

pp. 1107-1114 ◽

Cited By ~ 159

Author(s):

G. C. Y. Wang ◽

Y. Wang

Keyword(s):

16S Rrna ◽

Bacterial Species ◽

16S Rrna Genes ◽

Rrna Genes ◽

Chimeric Molecules

Kupffer Cell-targeting strategy for the protection of Hepatic Ischemia/Reperfusion Injury

Nanotechnology ◽

10.1088/1361-6528/abde02 ◽

2021 ◽

Author(s):

Qingqing Dai ◽

Wei Jiang ◽

Hu Liu ◽

Xin Qing ◽

Guobin Wang ◽

...

Keyword(s):

Reperfusion Injury ◽

Kupffer Cell ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Cell Targeting ◽

Hepatic Ischemia ◽

Hepatic Ischemia Reperfusion ◽

Targeting Strategy

Abstract 495: GSTM1 Deficiency Exacerbates Hypertension in the Remnant Model of Chronic Kidney Disease

Hypertension ◽

10.1161/hyp.62.suppl_1.a495 ◽

2013 ◽

Vol 62 (suppl_1) ◽

Author(s):

Sylvia Cechova ◽

Rosa Chan ◽

Beverly Koller ◽

Thu H Le

Keyword(s):

Oxidative Stress ◽

Chronic Kidney Disease ◽

Kidney Disease ◽

Null Allele ◽

Null Alleles ◽

Hypertensive Nephrosclerosis ◽

Baseline Systolic Blood Pressure ◽

Glutathione S Transferases ◽

Targeting Strategy ◽

Multiple Chronic Diseases

There is a general consensus that oxidative stress is a factor in the progression of chronic kidney disease (CKD). Hence, genetic variants that affect the capacity to handle oxidative stress may influence the outcomes of CKD. One important class of enzymes that has evolved to combat the damaging effects of reactive oxygen species is the glutathione-S-transferases. In particular, the μ class isoform 1 (GSTM1) has emerged as a potential modifier of multiple chronic diseases in humans. Approximately 30%-50% of humans are completely deficient of the GSTM1 enzyme because of homozygous inheritance of the GSTM1 null allele, GSTM1(0). We have identified the GSTM1 gene as a modifier of disease progression in hypertensive nephrosclerosis (HN). In an ancillary study of the African American (AA) Study of Hypertension and Kidney Disease (AASK) Trial, we reported that participants carrying one ( 1/0 ) or two ( 0/0 ) null alleles had 1.7- and 2-fold higher risk of the composite outcome of a 50% decline in the glomerular filtration rate (GFR), dialysis, or death relative to those with two active alleles. Here, the objective of our study was to determine the consequence of deletion of Gstm1 on the course of chronic kidney disease induced by reduction of renal mass (RRM) model in mice. We generated Gstm1-/- (KO) mice on the 129S6 background through conventional gene targeting strategy. By radiotelemetry, Gstm1 KO mice displayed a modest but significantly higher baseline systolic blood pressure (SBP) compared to their wild type (WT, Gtsm1 +/+ ) littermates: KO (n = 5): 138.8 ± 1.3; WT (n = 5): 132.1 ± 1.1, p < 0.01. Baseline urinary isoprostane (ng/100 mg of body weight) was significantly higher in KO mice than WT mice (15.1 ± 2.9; WT: 8.0 ± 0.8, p < 0.04). Four weeks after sub-total nephrectomy, Gstm1 KO mice developed significantly more severe hypertension than WT mice. The average SBP over a 2 week recording by radiotelemetry was 154.0 ± 3.2 mm Hg in KO mice (n = 5), and 142.3 ± 4.2 in WT mice (n = 3), p < 0.01. The effects of deletion of Gstm1 on kidney function and histopathology are under investigation. In conclusion, loss of GSMT1 increases oxidative stress and exaggerates hypertension in the murine model of chronic kidney disease.