Molecular and Cellular Biochemistry (MOL CELL BIOCHEM)

Publisher: Springer Verlag

Journal description

Molecular and Cellular Biochemistry: An International Journal for Chemical Biology in Health and Disease publishes original full-length research papers and short communications in all areas of the biochemical sciences the emphasis being on those papers which present novel findings relevant to the biochemical basis of cellular function and disease processes as well as the mechanics of action of hormones and chemical agents. Investigations directed towards molecular biology and gene expression in the cell are particularly encouraged. Membrane transport receptor mechanism immune response secretory processes and cytoskeletal function are areas of great interest to this journal as are articles in all areas related to biochemical structure-function relationships in the cell. Studies examining adaptation of biochemical processes at the molecular and cellular levels in response to physiological and pathological stimuli are welcome. In addition to the reports of original research the journal publishes state of the art reviews. Specific subjects that are covered by Molecular and Cellular Biochemistry are: cellular metabolism cellular pathophysiology enzymology ion transport lipid biochemistry membrane biochemistry molecular biology nuclear structure and function and protein chemistry.

Current impact factor: 2.39

Impact Factor Rankings

2016 Impact Factor Available summer 2017
2014 / 2015 Impact Factor 2.393
2013 Impact Factor 2.388
2012 Impact Factor 2.329
2011 Impact Factor 2.057
2010 Impact Factor 2.168
2009 Impact Factor 1.896
2008 Impact Factor 1.764
2006 Impact Factor 1.862
2005 Impact Factor 1.681
2004 Impact Factor 1.714
2003 Impact Factor 1.763
2002 Impact Factor 1.548
2001 Impact Factor 1.583
2000 Impact Factor 2.054
1999 Impact Factor 1.547
1998 Impact Factor 1.273
1997 Impact Factor 1.345
1996 Impact Factor 1.504
1995 Impact Factor 1.625
1994 Impact Factor 1.25
1993 Impact Factor 1.06
1992 Impact Factor 1.377

Impact factor over time

Impact factor
Year

Additional details

5-year impact 2.37
Cited half-life 7.30
Immediacy index 0.79
Eigenfactor 0.02
Article influence 0.60
Website Molecular and Cellular Biochemistry website
Other titles Molecular and cellular biochemistry
ISSN 0300-8177
OCLC 1787431
Material type Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

Publisher details

Springer Verlag

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Author's pre-print on pre-print servers such as arXiv.org
    • Author's post-print on author's personal website immediately
    • Author's post-print on any open access repository after 12 months after publication
    • Publisher's version/PDF cannot be used
    • Published source must be acknowledged
    • Must link to publisher version
    • Set phrase to accompany link to published version (see policy)
    • Articles in some journals can be made Open Access on payment of additional charge
  • Classification
    green

Publications in this journal


  • No preview · Article · Feb 2016 · Molecular and Cellular Biochemistry
  • [Show abstract] [Hide abstract]
    ABSTRACT: Ovarian cancer is a highly aggressive pathology, displaying a poor prognosis and chemoresistance to classical therapy. The present study was conducted to evaluate the effect of caffeic acid phenethyl ester (CAPE) on survival of ovarian cancer cell lines, A2780 (sensitive to cisplatin) and A2780cis (resistant to cisplatin). MTT assay was used to evaluate cell viability, while the apoptotic processes were examined by flow cytometry and qRT-PCR. A reduction of cell proliferation and activation of the apoptosis was observed in both cell lines. qRT-PCR evaluation demonstrated the activation of the pro-apoptotic genes (BAD, CASP8, FAS, FADD, p53) in both cell lines. The limited therapeutic effect in A2780 cells is explained by the activation of epithelial–mesenchymal transition-related genes (ZEB1, ZEB2, or TGFBB1) as displayed by Ingenuity Network analysis. Overall data suggest that CAPE can be used as an alternative in sensitizing cells to chemotherapy.
    No preview · Article · Feb 2016 · Molecular and Cellular Biochemistry
  • [Show abstract] [Hide abstract]
    ABSTRACT: The microbial polyketide, 2, 4-diacetylphloroglucinol (DAPG), exhibited a broad-spectrum of anti-leukemic, anti-lung, and anti-breast cancer properties. The aim of the present investigation was to study the interactive potentials of DAPG with the metastatic proteins such as MMP-2, MMP-9, and NF-κB and antiapoptotic Bcl-2 family proteins such as Bcl-2, Bcl-w, and Bcl-xL through in silico interaction and in vitro studies. The in silico modeling predicted high interactions of DAPG with the metastatic proteins, especially MMP-2, MMP-9, and NF-κB with the glide score of −7.028, −6.304, and −5.231, respectively. Similarly, the DAPG had weak interactions with the antiapoptotic Bcl-2, Bcl-w, and Bcl-xL with the glide score of −4.505, −3.839, and −4.003, respectively. The interaction studies further revealed the inhibition of MMP-2, MMP-9, and NF-κB activities with the low IC50 concentration of 5.82 ± 1.6, 6.74 ± 1.2, and 10.7 ± 1.5 μM respectively, in the presence of DAPG. Similarly, DAPG inhibited the Bcl-2, Bcl-xL and Bcl-w activities with the high IC50 concentration of 29.8 ± 1.9, 85.9 ± 2.7, and 97.4 ± 1.5 μM, respectively. These results correlate with the relatively high IC50 concentration of 16.3 ± 1.76, 7.67 ± 0.78, and 10.7 ± 0.96 μM in the Bcl-2-overexpressing HL-60, K562 and Raji leukemic cells than the metastatic A549 and MDA MB-231 cancer cells with the low IC50 concentration of 0.06 ± 0.02 and 0.08 ± 0.01 μM, respectively, compared to the healthy, human embryonic kidney (HEK-293) cells with the high IC50 concentration of 54.7 ± 1.43 μM. In summary, the affinity of DAPG with proteins are in the order of MMP-2 > MMP-9 > NF-κB > Bcl-2 > Bcl-xL > Bcl-w. Results presented in this study confirmed the high interaction of DAPG with the metastatic proteins than the antiapoptotic Bcl-2 family proteins.
    No preview · Article · Feb 2016 · Molecular and Cellular Biochemistry
  • [Show abstract] [Hide abstract]
    ABSTRACT: MicroRNAs (miRNAs) play essential roles in muscle cell proliferation and differentiation. The muscle-specific miRNAs miR-1 and miR-206 have been shown to regulate muscle development and promote myogenic differentiation; however, it is likely that a number of other miRNAs play important roles in regulating myogenesis as well. microRNA-128 (miR-128) has been reported to be highly expressed in brain and skeletal muscle, and we found that miR-128 is also up-regulated during bovine skeletal muscle satellite cell differentiation using microarray analysis and qRT-PCR. However, little is known about the functions of miR-128 in bovine skeletal muscle satellite cell development. In this study, we investigated the biological functions of miR-128 in bovine skeletal muscle cell development. Using a dual-luciferase reporter assay, we confirmed that miR-128 regulates the Sp1 gene. Over-expression of miR-128 reduced Sp1 protein levels and inhibited muscle satellite cell proliferation and differentiation. Inhibition of miR-128 increased Sp1 protein levels and promoted muscle satellite cell differentiation but also suppressed proliferation. Changes in miR-128 and Sp1 expression levels also affected the protein levels of MyoD and CDKN1A. Sp1, an activator of MyoD and a suppressor of CDKN1A, plays an important role in bovine muscle cell proliferation and differentiation. The results of our study reveal a mechanism by which miR-128 regulates bovine skeletal muscle satellite cell proliferation and myogenic differentiation via Sp1.
    No preview · Article · Feb 2016 · Molecular and Cellular Biochemistry
  • [Show abstract] [Hide abstract]
    ABSTRACT: Colorectal cancer is a critical health concern because of its incidence as the third most prevalent cancer in the world. Currently, 5-fluorouracil (5-FU), 6-thioguanine, and certain other genotoxic agents are mainstays of treatment; however, patients often die due to emergence of resistant population. Curcumin, a bioactive compound derived from the dietary turmeric (Curcuma longa) is an effective anticancer, anti-inflammatory, and antioxidant agent. Previously, we reported that human colorectal cancer cell lines compromised for mismatch repair (MMR) function exhibit heightened sensitivity to curcumin due to sustained curcumin-induced unrepaired DNA damage compared to proficient population counterparts. In this report, we show that the protein levels of gadd45α, whose transcript levels are increased during DNA damage and stress signals, are upregulated following curcumin treatment in a dose- and time-dependent manner. We further observed that cells compromised for Mlh1 function (HCT116 + Ch2) displayed ~twofold increased GADD45α upregulation compared to similarly treated proficient counterparts (HCT116 + Ch3). Similarly, suppression of Mlh1 using ShRNA increased GADD45α upregulation upon curcumin treatment. On the other hand, suppression of GADD45α using SiRNA-blocked curcumin-induced cell death induction in Mlh1-deficient cells. Moreover, inhibition of Abl through ST571 treatment and its downstream effector JNK through SP600125 treatment blocked GADD45α upregulation and cell death triggered by curcumin. Collective results lead us to conclude that GADD45α modulates curcumin sensitivity through activation of c-Abl > JNK signaling in a mismatch repair-dependent manner.
    No preview · Article · Jan 2016 · Molecular and Cellular Biochemistry
  • [Show abstract] [Hide abstract]
    ABSTRACT: Hypertensive cerebropathy is a pathological condition associated with cerebral edema and disruption of the blood–brain barrier. However, the molecular pathways leading to this condition remains obscure. We hypothesize that MMP-9 inhibition can help reducing blood pressure and endothelial disruption associated with hypertensive cerebropathy. Dahl salt-sensitive (Dahl/SS) and Lewis rats were fed with high-salt diet for 6 weeks and then treated without and with GM6001 (MMP inhibitor). Treatment of GM6001 (1.2 mg/kg body weight) was administered through intraperitoneal injections on alternate days for 4 weeks. GM6001 non-administered groups were given vehicle (0.9 % NaCl in water) treatment as control. Blood pressure was measured by tail-cuff method. The brain tissues were analyzed for oxidative/nitrosative stress, vascular MMP-9 expression, and tight junction proteins (TJPs). GM6001 treatment significantly reduced mean blood pressure in Dahl/SS rats which was significantly higher in vehicle-treated Dahl/SS rats. MMP-9 expression and activity was also considerably reduced in GM6001-treated Dahl/SS rats, which was otherwise notably increased in vehicle-treated Dahl/SS rats. Similarly MMP-9 expression in cerebral vessels of GM6001-treated Dahl/SS rats was also alleviated, as devised by immunohistochemistry analysis. Oxidative/nitrosative stress was significantly higher in vehicle-treated Dahl/SS rats as determined by biochemical estimations of malondialdehyde, nitrite, reactive oxygen species, and glutathione levels. RT-PCR and immunohistochemistry analysis further confirmed considerable alterations of TJPs in hypertensive rats. Interestingly, GM6001 treatment significantly ameliorated oxidative/nitrosative stress and TJPs, which suggest restoration of vascular integrity in Dahl/SS rats. These findings determined that pharmacological inhibition of MMP-9 in hypertensive Dahl-SS rats attenuate high blood pressure and hypertension-associated cerebrovascular pathology.
    No preview · Article · Jan 2016 · Molecular and Cellular Biochemistry
  • [Show abstract] [Hide abstract]
    ABSTRACT: VEGF-C is a newly identified proangiogenic protein playing an important role in vascular disease and angiogenesis. However, its role in myocardial ischemia/reperfusion (I/R) injury remains unknown. The objective of this study was to determine the role and mechanism of VEGF-C in myocardial ischemia–reperfusion injury. Rat left ventricle myocardium was injected with recombinant human VEGF-C protein (0.1 or 1.0 µg/kg b.w.) 1 h prior to myocardial ischemia–reperfusion (I/R) injury. 24 h later, the myocardial infarction size, the number of TUNEL-positive cardiomyocytes, the levels of creatine kinase (CK), CK-MB, cardiac troponin, malondialdehyde (MDA) content, and apoptosis protein Bax expression were decreased, while Bcl2 and pAkt expression were increased in VEGF-C-treated myocardium as compared to the saline-treated I/R hearts. VEGF-C also improved the function of I/R-injured hearts. In the H2O2-induced H9c2 cardiomyocytes, which mimicked the I/R injury in vivo, VEGF-C pre-treatment decreased the LDH release and MDA content, blocked H2O2-induced apoptosis by inhibiting the pro-apoptotic protein Bax expression and its translocation to the mitochondrial membrane, and consequently attenuated H2O2-induced decrease of mitochondrial membrane potential and increase of cytochrome c release from mitochondria. Mechanistically, VEGF-C activated Akt signaling pathway via VEGF receptor 2, leading to a blockade of Bax expression and mitochondrial membrane translocation and thus protected cardiomyocyte from H2O2-induced activation of intrinsic apoptotic pathway. VEGF-C exerts its cardiac protection following I/R injury via its anti-apoptotic effect.
    No preview · Article · Jan 2016 · Molecular and Cellular Biochemistry
  • [Show abstract] [Hide abstract]
    ABSTRACT: Lysosomes and peroxisomes are organelles with many functions in all eukaryotic cells. Lysosomes contain hydrolytic enzymes (lysozyme) that degrade molecules, whereas peroxisomes contain enzymes such as catalase that convert hydrogen peroxide (H2O2) to water and oxygen and neutralize toxicity. In contrast, melanin is known as a helpful element to protect the skin against harmful ultraviolet rays. However, a high quantity of melanin leads to hyperpigmentation or skin cancer in human. New materials have already been discovered to inhibit tyrosinase in melanogenesis; however, melanin reduction does not suggest their preparation. In this study, we report that the color intensity because of melanin decreased by the cellular activation of lysosomes and peroxisomes. An increase in the superficial intensity of lysosome and peroxisome activities of HeLa cells was observed. In addition, a decrease in the amount of melanin has also been observed in mammalian cells without using any other chemical, showing that the process can work in vivo for treating melanin. Therefore, the results of this study indicate that the amount of melanin decreases by the lysosome and peroxisome activity after entering the cells, and functional organelles are effective in color reduction. This mechanism can be used in vivo for treating melanin.
    No preview · Article · Jan 2016 · Molecular and Cellular Biochemistry
  • [Show abstract] [Hide abstract]
    ABSTRACT: Galectins, a family of soluble β-galactoside-binding proteins, are involved in the regulation of various cellular functions, which are essential for adaptive cellular stress responses (CSRs). Although expression patterns of galectins and galectin-binding glycans change during tissue development and cancer, the requirement and role of galectin networks in the CSRs are not completely understood. In this study, we report that the treatment of human promyelocytic HL-60 cells with stimuli mimicking hypoxia (CoCl2), inducing the endoplasmic reticulum stress (tunicamycin), and stimulating cell differentiation, result in stress-specific differential expression of galectin transcripts. In addition, we show that CoCl2 increases the expression of cell surface glycans recognized by both β-galactoside- and GlcNAc-binding lectins. Thus, microenvironmental stress changes the glycobiological status of cells representing expression profiles of endogenous lectins and corresponding glycans. These findings introduce a novel classification of galectins in HL-60 cells, which suggests diverse functions of galectin members in CSRs.
    No preview · Article · Jan 2016 · Molecular and Cellular Biochemistry
  • [Show abstract] [Hide abstract]
    ABSTRACT: Btg2, a member of a family of antiproliferative proteins, is involved in downregulation of the JAK2-Stat3 signaling pathway. Here, we present evidence that the inhibitory effect of Btg2 on adipogenesis is suppressed by the proadipogenic activity of the Stat3 signaling pathway. Btg2 expression fluctuates during adipogenic differentiation of preadipocytes. Btg2 is also expressed at different levels in fat tissues from lean and obese mice. Furthermore, knockdown of Btg2 expression enhanced lipid accumulation and upregulated the expression of adipogenic marker genes. To gain insights into the molecular mechanisms of Btg2 action in adipocytes, adipocytes were treated with previously identified bioactive compounds and the expression of Btg2 was assessed. This effort identified the small molecule WP1066, a known Stat3 inhibitor, as an inducer of Btg2 expression. In line with this observation, siRNA-mediated silencing of Stat3 resulted in upregulated Btg2 expression and decreased lipid accumulation. Furthermore, siRNA-mediated silencing of Btg2 attenuated WP1066-mediated inhibition of adipocyte differentiation. We discuss a model for the role of Btg2 in adipogenesis and propose that Btg2 and Stat3 act in a functional hierarchy.
    No preview · Article · Jan 2016 · Molecular and Cellular Biochemistry
  • [Show abstract] [Hide abstract]
    ABSTRACT: Tunicamycin (TM) is an inducer of endoplasmic reticulum (ER) stress. However, which genes related to ER stress was induced in cardiomyocytes on a genome-wide scale remains poorly understood. Salubrinal and its derivatives are ER stress inhibitors. However, the cellular protection mechanisms remain unresolved. Neonatal rat cardiomyocytes were cultured from ventricles of one-day-old Wistar rats. Cells were exposed to salubrinal, its derivatives (PP1-12, PP1-24) or vehicle followed by TM treatment at different times. Total RNA was isolated from cells for RNA-sequencing analysis. The expressions of 189, 182, 556, 860, and 1314 genes were changed in cells exposed to TM for 1, 3, 6, 12, and 24 h. Five well-known UPR genes (Hspa5, Hsp90b1, Calr, Ddit3, and Atf4) were significantly increased in a time-dependent manner. Six not well-known genes (Hyou1, Herpud1, Manf, Creld2, Sdf2l1, and Slc3a2) were highlighted to be involved in ER stress. Compared with TM-only treated cells, the expressions of 36 genes upregulated by TM and 74 genes downregulated by TM were reversed by salubrinal. In comparison, 121 genes upregulated by TM and 92 genes downregulated by TM were reversed by PP1-12. Most genes altered by salubrinal are in the category of transcription (1 h) and cell cycle (24 h). Most genes altered by PP1-12 are in the category of response to ER stress (3 h) and cell cycle (24 h). Our findings help elucidate the mechanism for TM treatment and may be useful for future drug screens involved in ER stress.
    No preview · Article · Jan 2016 · Molecular and Cellular Biochemistry
  • [Show abstract] [Hide abstract]
    ABSTRACT: N6-benzyladenine and kinetin are adenine-type cytokinins that play various roles in many aspects of plant development and stimulate anabolic processes in plant cells. The aim of this study was to examine the effect of N6-benzyladenine and kinetin on basic oxidative stress parameters, such as antioxidative enzyme activity, reduced glutathione and thiol group content, and lipid peroxidation. The results show a stimulatory effect of kinetin and N6-benzyladenine on antioxidative enzyme activity, as well as reduced glutathione and thiol group content. Cytokinins caused a decrease in membrane phospholipid peroxidation and exhibited protective properties against malondialdehyde production. The present findings reveal that both N6-benzyladenine and kinetin exhibit multiple and complex actions in fibroblast cells in vitro. Both show antioxidant properties and are potentially powerful agents with applications in the prevention and treatment of many diseases connected with oxidative stress in skin, for example, psoriasis.
    No preview · Article · Jan 2016 · Molecular and Cellular Biochemistry
  • [Show abstract] [Hide abstract]
    ABSTRACT: Soluble fms-like tyrosine kinase-1 (sFlt-1) functions as a potent inhibitor of angiogenesis by trapping vascular endothelial growth factor (VEGF). However, the precise regulatory mechanism of sFlt-1 production is unknown. Here, we report that vascular sFlt-1 production is regulated by heterogeneous nuclear ribonucleoprotein D (hnRNP D) and arginine methylation. We showed that hnRNP D bound to Flt-1 pre-mRNA and that hnRNP D overexpression decreased sFlt-1 mRNA in human microvascular endothelial cells (HMVECs). In contrast, the reduction of hnRNP D levels induced an increase in sFlt-1 production. Overexpression of an hnRNP D mutant in which the arginine residue of the known arginine methylation motif (arginine-glycine-glycine; RGG) was replaced with alanine did not reduce the level of soluble-form RNA produced from the Flt-1 minigene. Moreover, we demonstrated that overexpression of arginine methyltransferase decreased the soluble-form RNA level, whereas overexpression of arginine demethylase and addition of methyltransferase inhibitors increased sFlt-1 mRNA levels. These findings indicate that hnRNP D and arginine methylation play important roles in the regulation of Flt-1 mRNA alternative polyadenylation.
    No preview · Article · Jan 2016 · Molecular and Cellular Biochemistry
  • [Show abstract] [Hide abstract]
    ABSTRACT: Hypertrophic scar (HS) is characterized by excessive fibrosis associated with aberrant function of fibroblasts. Currently, no satisfactory drug has been developed to treat the disease. Here we found that a flavonoid natural product, galangin, could significantly attenuate hypertrophic scar formation in a mechanical load-induced mouse model. Both in vivo and in vitro studies demonstrated that galangin remarkably inhibited collagen production, proliferation, and activation of fibroblasts. Besides, galangin suppressed the contractile ability of hypertrophic scar fibroblasts. Further Western blot analysis revealed that galangin dose-dependently down-regulated Smad2 and Smad3 phosphorylation. Such bioactivity of galangin resulted from its selective targeting to the activin receptor-like kinase 5 (ALK5) was demonstrated by ALK5 knockdown and over-expression experiments. Taken together, this compound could simultaneously inhibit both the accumulation of collagen and abnormal activation/proliferation of fibroblasts, which were the two pivotal factors for hypertrophic scar formation, thus suggesting that galangin serves as a potential agent for treatment of HS or other fibroproliferative disorders.
    No preview · Article · Jan 2016 · Molecular and Cellular Biochemistry