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The Potential of Microbial Mediated Fermentation Products of Herbal Material in Anti-Aging Cosmetics
Published in Namrita Lall, Medicinal Plants for Cosmetics, Health and Diseases, 2022
Type III collagen comprises approximately 20% of the total collagen in the skin, concentrated in the mesh-like papillary dermis, while the remaining 80% is comprised of type-I collagen, concentrated in the reticular dermis. Structurally, type III collagen is a homotrimer of α1(III) chains and type I, a heterotrimer of two α1(I) chains and one α2(I) chain arranged in an anti-parallel conformation to produce more dense fibers (Cole et al., 2018). These fibers are enzymatically cross linked following the secretion of procollagen and its maturation to confer resistance to proteolytic cleavage. The proteolytic removal of C and N terminal pro-peptides facilitates the maturation of procollagen into mature collagen fibers. For instance, in type-I collagen various intracellular lysine residues containing α1(I) and α2(I) chains are converted to hydroxylysine through the action of lysyl hydroxylase, while extracellular lysine and hydroxylysine residues are converted to aldehydes through the action of lysyl oxidase. This process enables spontaneous, non-reducible inter- and intra-peptide crosslinking. The action of lysyl oxidase is crucial in facilitating matrix deposition of elastin fibers and prevention of excessive elasticity (Cole et al., 2018).
Drug Targeting to the Lung: Chemical and Biochemical Considerations
Published in Anthony J. Hickey, Sandro R.P. da Rocha, Pharmaceutical Inhalation Aerosol Technology, 2019
Peter A. Crooks, Narsimha R. Penthala, Abeer M. Al-Ghananeem
Idiopathic pulmonary fibrosis (IPF) is a fatal lung disease with few options for treatment (Kim et al. 2006), since the aetiology of the disease is poorly understood. It has a 5-year survival rate of 30%–50%. Recent studies have shown that accumulation of extracellular matrix plays an important role in IPF, and repeated alveolar injury causes fibroblast activation, proliferation, and differentiation myofibroblasts (Wolters et al. 2014, Blackwell et al. 2014). The myofibroblasts overgrow the alveolar lung tissue, and this results in an irreversible increase in the amounts of extracellular matrix (Parker et al. 2014). Current therapeutic interventions involve targeting matrix and matrix-processing enzymes, and inhibition of the collagen cross-linking enzyme, lysyl oxidase-like 2 is currently being investigated as a treatment option for IPF (Ahluwalia et al. 2014). The FDA approved drugs pirfenidone and nintedanib are also being utilized to treat IPF (King et al. 2014, Richeldi et al. 2014). It is known that a deficiency in the chaperone protein, FK506-binding protein 10 can attenuate collagen secretion and decrease extracellular collagen cross-linking, and this might provide a potentially specific and effective drug for treatment of IPF (Staab-Weijnitz et al. 2015).
For The Want of a Nail … Trace Elements in Health and Disease
Published in Owen M. Rennert, Wai-Yee Chan, Metabolism of Trace Metals in Man, 2017
Paul Saltman, Jack Hegenauer, Linda Strause
Copper is in many respects analogous to iron in its redox reactions. There is a facile equilibrium between the oxidized, Cu2+, and the reduced form, Cu1+ . In a cooperative mechanism, copper functions with the iron of cytochrome a3, the critical terminal step in the aerobic electron transport system of mitochondria. Several hydroxylation and oxidation reactions are copper mediated. The Cu-containing enzyme tyrosinase is responsible for synthesizing the black skin and hair pigment, melanin, by hydroxylation and oxidation of tyrosine. Therefore, the color of some sheep wool can be correlated directly with the copper status of the animal. Lysyl oxidase is involved in the cross-linking and strengthening of collagen and elastin. In the absence of copper, major defects are observed in heart muscle, vascular tissue, and the organic matrix of bone which in turn leads to skeletal abnormalities.4 The importance of copper enzymes in brain metabolism has been shown for many species. For example, the inability to coordinate nerve and muscle (ataxia) has been linked with a lower level of copper enzymes involved in the synthesis of myelin, the insulating sheath of nerve cells. Copper is necessary to maintain proper concentrations of bioamines such as dopamine, epinephrine, and norepinephrine.
Isonicotinic acid hydrazide (INH) versus extra-amniotic saline infusion (EASI) for cervical ripening at term: a randomised controlled trial
Published in Journal of Obstetrics and Gynaecology, 2022
Ladan Haghighi, Behnaz Mohabbatian, Zahra Najmi, Samaneh Rokhgireh, Samira Saadatjoo, Yousef Moradi, Mojgan Mokhtari
Isonicotinic acid hydrazide, an anti-tuberculosis agent, is recently introduced as a cervical ripening agent (Haghighi and Mohabatian 2015; Haghighi et al. 2020). It acts via increasing collagen solubility due to inactivation of lysyl oxidase, which is responsible for initiation of cross-link formation in collagen (Carrington et al. 1984). Moreover, it has been suggested that INH may cause lysyl oxidase inhibition by competing for its obligatory cofactor, pyridoxal phosphate (Carrington et al. 1984). Reduction in collagen cross-linking has been shown to decrease mechanical strength of the resulting tissue (Mahendroo 2012). Finding an agent for cervical ripening without stimulating uterine contractions is ideal and the advantage of INH is the possibility to be used in the outpatient setting with no need for foetal monitoring and also in patients with prior caesarean section. In this randomised clinical trial, we compared the efficacy of isonicotinic acid hydrazide and EASI for pre-induction cervical ripening among women with term pregnancy and unfavourable cervix.
Co-administration of resveratrol and beta-aminopropionitrile attenuates liver fibrosis development via targeting lysyl oxidase in CCl4-induced liver fibrosis in rats
Published in Immunopharmacology and Immunotoxicology, 2019
Roohollah Mohseni, Zahra Arab Sadeghabadi, Mohammad Taghi Goodarzi, Jamshid Karimi
The regression of liver fibrosis has become one of the most important challenge facing scientists in recent years [5]. In terms of molecular aspect, lysyl oxidase (LOX) enzyme plays a critical role in the pathogenesis of liver fibrosis. High secretion and activity of LOX limit regression of liver fibrosis [6]. For this reason, downregulation and inhibition of the LOX enzyme can facilitate regression of liver fibrosis. For this reason, targeting the expression and function of LOX can be a new therapeutic approach for inhibiting hepatic fibrosis progression. Although, a recent study showed the selective inhibition of this enzyme by anti-LOX monoclonal antibody (simtuzumab) is not promising [7]. Also, it has been associated with the side effects including dyspnea, cough, and upper respiratory tract infection. On the other hand, the irreversible inhibition of LOX by beta-aminopropionitrile (BAPN) decreased the tissue stiffness by inhibiting collagen crosslinking in liver fibrosis but could not improve liver inflammation [6,7].
Recent advances in molecular biomarkers for patients with hepatocellular carcinoma
Published in Expert Review of Molecular Diagnostics, 2019
Shinichi Umeda, Mitsuro Kanda, Yasuhiro Kodera
The main function of lysyl oxidase like 2 (LOXL2) is to catalyze the covalent cross-linkage of collagen and elastin in the extracellular matrix [35]. Wang et al. investigated 201 HCC tissue samples and revealed that elevated LOXL2 expression was associated with an increase in tumor grade, vasculogenic mimicry and poor overall survival [27]. They also found a significant correlation between the levels of LOXL2 and HIF1α in clinical samples. They found that silencing HIF1α reduced LOXL2 expression and that migration and invasion were suppressed by shRNA knock-down of HIF1α and LOXL2. However, when LOXL2 was overexpressed in HIF-1α knockdown cells, cell functions returned to their original state. Analysis of EMT-related molecules showed that expression of VE-cadherin, a vascular mimicry marker, was increased when LOXL2 was overexpressed. Furthermore, transcriptome analysis revealed that the expression of HLTF, CENPF, ASPM, NIPBL, SLK, PIK3C2A, SMC2, TAF9B, and ATAD2 were upregulated by LOXL2 overexpression [27]. They concluded that HIF1α promotes LOXL2 expression and subsequent induction of EMT and vascular mimicry in HCC cells, thus promoting HCC progression. LOXL2 is, therefore, a promising therapeutic target for HCC.