Biomedical subjects

Xiang Qian

Publications and source records attributed to Xiang Qian.

At least 19 recordsLinked to original sources

PubMed2006

SK channels mediate NADPH oxidase-independent reactive oxygen species production and apoptosis in granulocytes.

Neutrophils are immune cells that bind to, engulf, and destroy bacterial and fungal pathogens in infected tissue, and their clearance by apoptosis is essential for the resolution of inflammation. Killing involves both oxidative and nonoxidative processes, the oxidative pathway requiring electrogenic production of superoxide by the membrane-bound NADPH oxidase complex. A variety of stimuli, from bacterial chemotactic peptides to complement- or IgG-opsonized microbes, can induce the production of reactive oxygen species (ROS) by neutrophils, presumably by means of NADPH oxidase. We report here that 1-ethyl-2-benzimidazolinone (1-EBIO), an activator of Ca2+-activated potassium channels of small conductance (SK) and intermediate conductance (IK), causes production of superoxide and hydrogen peroxide by neutrophils and granulocyte-differentiated PLB-985 cells. This response can be partially inhibited by the SK blocker apamin, which inhibits a Ca2+-activated K+ current in these cells. Analysis of RNA transcripts indicates that channels encoded by the SK3 gene carry this current. The effects of 1-EBIO and apamin are independent of the NADPH oxidase pathway, as demonstrated by using a PLB-985 cell line lacking the gp91phox subunit. Rather, 1-EBIO and apamin modulate mitochondrial ROS production. Consistent with the enhanced ROS production and K+ efflux mediated by 1-EBIO, we found that this SK opener increased apoptosis of PLB-985 cells. Together, these findings suggest a previously uncharacterized mechanism for the regulation of neutrophil ROS production and programmed cell death.

Apamin↗

PubMed2006

K+ channel selectivity depends on kinetic as well as thermodynamic factors.

Potassium channels are necessary for a number of essential biological tasks such as the generation of action potentials and setting the resting membrane potential in cells, both of which require that these channels selectively permit the passage of potassium ions while suppressing the flow of other ions. Generally, this selectivity is attributed to a narrow stretch of the channel known as the selectivity filter. Over this stretch ions are dehydrated, and the backbone oxygen atoms of the protein mimic the ion's loss of coordination by water. However, channels are long pores with spatially distinct ion-binding sites that all must be traversed during ion permeation. We have shown that selectivity of mutant Kir3.2 (GIRK2) channels can be substantially amplified by introducing acidic residues into the cavity, a binding site below the selectivity filter. Here, we carry out electrostatic calculations on homology models to quantify the degree of stabilization that these mutations have on ions in the cavity. We then construct a multiion model of ion permeation to calculate the channel's permeability to potassium relative to sodium. This kinetic model uses rates derived from the electrostatic calculations and demonstrates that nonselective electrostatic stabilization of cations in the cavity can amplify channel selectivity independently of the selectivity filter. This nonintuitive result highlights the dependence of channel properties on the entire channel architecture and suggests that selectivity may not be fully understood by focusing solely on thermodynamic considerations of ion dehydration and the energetics of the selectivity filter.

Amino Acids↗

PubMed2006

Modulation of basal and receptor-induced GIRK potassium channel activity and neuronal excitability by the mammalian PINS homolog LGN.

G protein-activated inwardly rectifying potassium (GIRK) channels mediate slow synaptic inhibition and control neuronal excitability. It is unknown whether GIRK channels are subject to regulation by guanine dissociation inhibitor (GDI) proteins like LGN, a mammalian homolog of Drosophila Partner of Inscuteable (mPINS). Here we report that LGN increases basal GIRK current but reduces GIRK activation by metabotropic transmitter receptors coupled to Gi or Go, but not Gs. Moreover, expression of its N-terminal, TPR-containing protein interaction domains mimics the effects of LGN in mammalian cells, probably by releasing sequestered endogenous LGN. In hippocampal neurons, expression of LGN, or LGN fragments that mimic or enhance LGN activity, hyperpolarizes the resting potential due to increased basal GIRK activity and reduces excitability. Using Lenti virus for LGN RNAi to reduce endogenous LGN levels in hippocampal neurons, we further show an essential role of LGN for maintaining basal GIRK channel activity and for harnessing neuronal excitability.

Animals↗

PubMed2006

Collapsing and non-collapsing focal segmental glomerulosclerosis in kidney transplants.

BACKGROUND: The aetiological and clinical associations of collapsing focal segmental glomerulosclerosis (cFSGS) following kidney transplantation (KTx) are poorly described. In this study, post-transplant cFSGS and non-collapsing FSGS (ncFSGS) were compared in recent KTx recipients. Evidence for intragraft viral infection was sought. METHODS: Twenty-nine cases of post-KTx FSGS were identified and classified as cFSGS (n = 10) or ncFSGS (n = 19). Biopsies were scored using Banff '97 criteria and subjected to in situ hybridization (ISH) for parvovirus B19 (pvB19), simian virus 40 (SV40) and BK virus (BKV). RESULTS: cFSGS and ncFSGS patients were comparable for age, gender, weight, delayed function, human leucocyte antigen (HLA) matching, acute rejection and median time to diagnosis. Deceased donor source was more common among cFSGS cases (70 vs 32%, P = 0.05). FSGS was recurrent in 2/10 cFSGS cases compared with 8/19 ncFSGS (P = NS). cFSGS was associated with more proteinuria (11.9 vs 7.2 g/day, P = 0.05) and higher serum creatinine (4.2 vs 1.9 mg/dl, P = 0.0001) at diagnosis. Plasmapheresis was used in two out of 10 cFSGS and seven out of 19 ncFSGS cases with treatment response in 0 of two and three of seven, respectively. Graft loss was more rapid with cFSGS compared with ncFSGS (P = 0.02). Histologically, cFSGS was associated with more severe chronic vascular abnormalities. All biopsies were negative for pvB19, SV40 and BKV by ISH. CONCLUSIONS: cFSGS following KTx presents with higher proteinuria, diminished renal function, more severe vascular disease and higher rate of graft loss compared with the non-collapsing form. There was no evidence for infection by pvB19 or polyomaviruses.

Adult↗

PubMed2006

Intra- and intersubunit cooperativity in activation of BK channels by Ca2+.

The activation of BK channels by Ca(2+) is highly cooperative, with small changes in intracellular Ca(2+) concentration having large effects on open probability (Po). Here we examine the mechanism of cooperative activation of BK channels by Ca(2+). Each of the four subunits of BK channels has a large intracellular COOH terminus with two different high-affinity Ca(2+) sensors: an RCK1 sensor (D362/D367) located on the RCK1 (regulator of conductance of K(+)) domain and a Ca-bowl sensor located on or after the RCK2 domain. To determine interactions among these Ca(2+) sensors, we examine channels with eight different configurations of functional high-affinity Ca(2+) sensors on the four subunits. We find that the RCK1 sensor and Ca bowl contribute about equally to Ca(2+) activation of the channel when there is only one high-affinity Ca(2+) sensor per subunit. We also find that an RCK1 sensor and a Ca bowl on the same subunit are much more effective in increasing Po than when they are on different subunits, indicating positive intrasubunit cooperativity. If it is assumed that BK channels have a gating ring similar to MthK channels with alternating RCK1 and RCK2 domains and that the Ca(2+) sensors act at the flexible (rather than fixed) interfaces between RCK domains, then a comparison of the distribution of Ca(2+) sensors with the observed responses suggest that the interface between RCK1 and RCK2 domains on the same subunit is flexible. On this basis, intrasubunit cooperativity arises because two high-affinity Ca(2+) sensors acting across a flexible interface are more effective in opening the channel than when acting at separate interfaces. An allosteric model incorporating intrasubunit cooperativity nested within intersubunit cooperativity could approximate the Po vs. Ca(2+) response for eight possible subunit configurations of the high-affinity Ca(2+) sensors as well as for three additional configurations from a previous study.

Algorithms↗

PubMed2006

BRAF mutation analysis in fine needle aspiration (FNA) cytology of the thyroid.

BRAF mutations have been detected in 30% to 80% of papillary thyroid carcinomas (PTC). Several detection methods for BRAF mutation have been reported, but a direct comparison between different assay methods has not been previously reported. In this study, we examined the diagnostic utility of BRAF (T1799A) mutation in 71 cases of thyroid fine needle aspiration specimens using 4 different methods, including direct sequencing, Colorimetric Mutector Assay, real-time LightCycler polymerase chain reaction (LC PCR) with fluorescence resonance energy transfer probes, and an allele-specific LC PCR with CYBR green 1. BRAF mutation was detected in 31 of 58 cases of PTC, but not in 13 cases of non-PTC lesions. The 4 assay methods used in this study were sensitive, reliable, and comparable with each other (100% of specificity and 53.5% of sensitivity). PTC harboring BRAF mutation had higher extrathyroidal invasion and/or lymph node metastasis than PTC with wild-type BRAF. BRAF mutation analysis should be useful for the clinical diagnosis of PTC in cases of indeterminate fine needle aspiration specimen, because of the high degree of specificity. Our results indicate that there is similar sensitivity for the four detection methods. However, the allele-specific LC PCR with CYBR green 1 method is most rapid, easier to perform, and least expensive technique, and it can be readily performed in most molecular diagnostic laboratories.

Adult↗

PubMed2006

Patterns of gene expression in pituitary carcinomas and adenomas analyzed by high-density oligonucleotide arrays, reverse transcriptase-quantitative PCR, and protein expression.

Very few of the genes that are important in pituitary tumor initiation, progression, and metastasis have been identified to date. To identify potential genes that may be important in pituitary tumor progression and carcinoma development, we used Affymetrix GeneChip HGU-133A-oligonucleotide arrays, which contain more than 15,000 characterized genes from the human genome to study gene expression in an ACTH pituitary carcinoma metastatic to the liver and four pituitary adenomas. Reverse-transcriptase real-time quantitative- PCR (RT-qPCR) was then used to analyze 4 nonneoplastic pituitaries, 19 adenomas, and the ACTH carcinoma. A larger series of pituitary adenomas and carcinomas were also analyzed for protein expression using tissue microarrays (TMA) (n = 233) and by Western blotting (n = 18). There were 4298 genes that were differentially expressed among the adenomas compared to the carcinoma, with 2057 genes overexpressed and 2241 genes underexpressed in the adenomas. The beta-galactoside binding protein galactin-3 was underexpressed in some adenomas compared to the carcinomas. Prolactin (PRL) and ACTH tumors had the highest levels of expression of galectin-3. The human achaetescute homolog-1 ASCL1 (hASH-1) gene was also underexpressed in some adenomas compared to the carcinoma. Prolactin and ACTH tumors had the highest levels of expression of hASH-1. ID2, which has an important role in cell development and tumorigenesis, was underexpressed in some adenomas compared to the carcinomas. Transducin-like enhancer of split four/ Groucho (TLE-4) was over-expressed in adenomas compared to the ACTH carcinoma. The differential expression of these genes was validated by RT-qPCR, by immunohistochemistry using TMA and by Western blotting. These results indicate that the LGALS3, hASH1, ID2, and TLE-4 genes may have important roles in the development of pituitary carcinomas.

ACTH-Secreting Pituitary Adenoma↗

PubMed2005

Effects of DNA methylation on galectin-3 expression in pituitary tumors.

Galectin-3 (Gal-3), a beta-galactoside-binding protein is expressed in a specific cell-type manner in pituitary tumors. Here we questioned the mechanism of Gal-3 expression in pituitary tumors, by using methylation-specific PCR and DNA sequence analyses to analyze the methylation status of the promoter region of the LGALS3 gene. DNA analysis of a human pituitary tumor, breast carcinoma cell lines, and thyroid carcinoma cell lines showed that in cells expressing Gal-3 protein, the LGALS3 gene was unmethylated, whereas in Gal-3 null cells, the promoter of the LGALS3 gene was methylated. Treatment of cells with 30 mumol/L 5-aza-2'-deoxycytidine induced Gal-3 mRNA and protein expression. Among pituitary tumors, 30% (7/23), mainly in follicle-stimulating hormone/luteinizing hormone-producing (38%) and null cell (57%) adenomas, the promoter of the LGALS3 was found to be methylated and silenced, although prolactin- and adrenocorticotropic hormone-producing tumors, which were unmethylated, expressed the Gal-3 protein. These results show for the first time that Gal-3 expression is regulated in part by promoter methylation in pituitary as well as in other tumors. Because it is functionally involved in cancer progression and metastasis, Gal-3 may serve as a possible therapeutic target in the treatment of pituitary tumors.

Adenoma↗

PubMed2005

RASSF1A and NORE1A methylation and BRAFV600E mutations in thyroid tumors.

We analyzed RASSF1A and NORE1A methylation and BRAF mutation in 89 thyroid tumors, 42 non-neoplastic thyroid tissues and three thyroid tumor cell lines using polymerase chain reaction (PCR), methylation-specific PCR, Western blotting and DNA sequencing in order to study thyroid tumor pathogenesis and progression. RASSF1A promoter methylation was present in all three thyroid cell lines and in 27/78 (35%) of benign and malignant thyroid tumors. We showed for the first time that there was generally good agreement between RASSF1A methylation status and RASSF1A protein expression. We also examined for the first time NORE1A promoter region methylation in thyroid cell lines and primary tumors and showed that two of three thyroid cell lines were methylated in the NORE1A promoter region, while all primary thyroid tumors analyzed (n=51) were unmethylated. BRAF mutation was present in 38% of papillary thyroid carcinomas (PTC), including 20% of PTC with a follicular variant pattern and 67% of the tall cell variant of PTC. Hyalinizing trabecular tumors (n=23), which had nuclear features similar to PTC, did not have BRAF mutations, indicating that the presence of BRAF mutations can help to separate these two tumor types. Phospho-MEK expression was increased in the NPA cell line, which had a BRAF mutation, supporting the importance of the BRAF pathway alterations in PTC pathogenesis. These results indicate that RASSF1A epigenetic changes are an early event in thyroid tumor pathogenesis and progression and that NORE1A methylation is uncommon in primary thyroid tumors. BRAF mutation occurs later in thyroid tumor progression and is restricted mainly to PTC and anaplastic thyroid carcinoma.

Adaptor Proteins, Signal Transducing↗

PubMed2005

Diagnosis of cat scratch disease with Bartonella henselae infection in formalin-fixed paraffin-embedded tissues by two different PCR assays.

Cat scratch disease (CSD) is commonly caused by Bartonella henselae infection. Clinical history and histologic findings are often insufficient to establish a definitive diagnosis of CSD. We retrospectively studied formalin-fixed, paraffin-embedded (FFPE) lymph nodes from 35 patients with histologically suspected CSD by 2 different PCR assays and immunohistochemistry (IHC). The first primer pair amplified a 163-bp fragment of the 16S rRNA gene in 19 of the 35 cases (54%). The second primer pair amplified a 191-bp fragment of the henselae citrate synthase (gltA) gene in 17 of the 35 cases (49%). IHC identified the organisms in 8 of 33 cases (24%). Fresh cultures of various Bartonella species showed a specific PCR product with an analytical sensitivity of 0.5 to 5 pg bacterial DNA. Bartonella species were identified by the unique size of the amplified PCR product. Twenty-two lymph nodes without morphologic evidence or a history of CSD were negative by PCR and immunostaining. Tissues from a patient with Legionella pneumophila were also negative by PCR and immunostaining for CSD supporting the specificity of the PCR reaction. The specific PCR products of the B. henselae were confirmed by sequencing. Human beta-actin for each case was amplified to check the integrity of the DNA. Our data indicate that detection of Bartonella DNA by PCR is useful to confirm the diagnosis of CSD.

Actins↗

PubMed2005

Molecular diagnosis of Ewing's sarcoma/primitive neuroectodermal tumor in formalin-fixed paraffin-embedded tissues by RT-PCR and fluorescence in situ hybridization.

Recent studies have suggested that formalin-fixed paraffin-embedded (FFPE) tissues can be used for molecular analyses by fluorescence in situ hybridization (FISH) and RT-PCR. We analyzed 18 cases of ES/PNET for the t(11;22)(q24;q12) and t(21;22)(q22;q12) fusion transcripts by RT-PCR and analyzed for EWS translocation by interphase FISH with a dual color fusion probe to compare these two approaches directly. RT-PCR detected 13 (72%) EWS-FLI-1 fusions (type I=10, type II=3) and 2 (11%) EWS-ERG fusions. Three cases could not be evaluated because the housekeeping gene phosphoglycerate kinase (internal mRNA control) was not amplified. FISH was diagnostic in 15 of 18 cases (83%). There were three discordant cases between RT-PCR and FISH (concordance of 83%). Using a combination of RT-PCR and FISH, the results were complementary. One advantage of RT-PCR analysis was that subtypes of EWS translocation could be determined specifically (type I, type II and ERG). These findings indicate that because of the difficulties and limitations associated with the molecular analysis of FFPE tissues, a combination of RT-PCR and FISH may be a better approach to enhance the sensitivity and accuracy of detecting ES/PNET translocations in FFPE tissues with suboptimally preserved nucleic acids.

Base Sequence↗

PubMed2005

Analysis of pituitary cells by laser capture microdissection.

The anterior pituitary gland consists of a heterogeneous population of various cell types. To study a single cell type with a homogeneous cell population, one can perform laser capture microdissection (LCM). Because different pituitary cells have unique immunophenotypic profiles, it is possible to perform immunohistochemical staining before LCM (immuno-LCM) for the collection of a phenotypically homogeneous cell population. These techniques were developed and applied to dissociated anterior pituitary cells and cultured pituitary cells. When combined with reverse transcriptase polymerase chain reaction, it is possible to analyze gene expression in as few as one to 10 pituitary cells. We have used the immuno-LCM technique to prepare homogeneous populations of folliculostellate cells. These cells were analyzed for expression of peptides and receptors. Anterior pituitary hormones were not expressed by these cells. These results show the utility of immuno-LCM for cellular and molecular studies of gene expression.

Animals↗

PubMed2005

DNA microarrays: recent developments and applications to the study of pituitary tissues.

Many new techniques are rapidly being developed and applied to the study of normal and neoplastic pituitary. DNA microarrays are a uniquely efficient method for simultaneously assessing the expression levels of thousands of genes, identifying disease subphenotypes, and predicting disease progression. This article reviews the utility of DNA microarray-based tumor profiling including recent developments and applications to pituitary biology in order to demonstrate how these new techniques are providing insights about basic aspects, clinical knowledge, and pharmacologic knowledge of the pituitary gland and about pituitary tumors.

Adenoma↗

PubMed2005

[Complete HBV DNA clone and sequence from serum samples of severe hepatitis B patients].

OBJECTIVE: To study the association between hepatitis B virus (HBV) mutants and the pathogenesis of severe hepatitis B by full-length HBV genome. METHODS: Serum samples from 10 severe hepatitis B patients were collected in our hospital. Serum HBV DNAs were extracted using DNA mini Kit, and amplified by LA Taq DNA polymerase to yield full-length HBV DNA. PCR products were isolated and cloned into vector pUCm-T, then transfected into DH-5 alpha cells. Positive clones were selected and checked by digestion, and full-length HBV DNAs were sequenced. RESULTS: 4 cases were cloned into vector pUCm-T successfully and completed the full-length sequencing. Among them, 3 cases had a G to A mutation at nucleotide 1896 in pre-C region and 1 had a double mutation of T1762-A1764 in the core promoter region. Some amino acid changes occurred within the known CTL, B or T cell epitopes of the PrS2 and C regions. CONCLUSIONS: This method could serve to study the relationship between HBV genome and the pathogenesis of severe hepatitis B.

Adult↗

PubMed2004

Linker-gating ring complex as passive spring and Ca(2+)-dependent machine for a voltage- and Ca(2+)-activated potassium channel.

Ion channels are proteins that control the flux of ions across cell membranes by opening and closing (gating) their pores. It has been proposed that channels gated by internal agonists have an intracellular gating ring that extracts free energy from agonist binding to open the gates using linkers that directly connect the gating ring to the gates. Here we find for a voltage- and Ca(2+)-activated K+ (BK) channel that shortening the linkers increases channel activity and lengthening the linkers decreases channel activity, both in the presence and absence of intracellular Ca2+. These observations are consistent with a mechanical model in which the linker-gating ring complex forms a passive spring that applies force to the gates in the absence of Ca2+ to modulate the voltage-dependent gating. Adding Ca2+ then changes the force to further activate the channel. Both the passive and Ca(2+)-induced forces contribute to the gating of the channel.

Allosteric Regulation↗

PubMed2004

Detection of hepatitis C virus RNA in formalin-fixed paraffin-embedded sections with digoxigenin-labeled cRNA probes.

Although recent studies have analyzed Hepatitis C (HCV) infections in liver tissue by in situ hybridization (ISH), many of these studies have been of limited diagnostic utility because of the low copy numbers of HCV in formalin-fixed paraffin-embedded (FFPE) tissue and failure to correlate the ISH analysis with other methods of detecting HCV. Thirty six cases of liver biopsies from patients with known HCV antibody status including 20 cases of serum HCV positive and 16 cases of serum HCV negative were analyzed. All cases showed histologic features suggestion of HCV infection. Analyses of all 36 cases were done by RT-PCR combined with Southern hybridization (RT-PCR-SH) and in situ hybridization (ISH). A prolactin riboprobe was used as a negative control. Immunohistochemistry (IHC) with an antibody against HCV (Rb 246) was also used to analyze HCV viral protein in the tissues. Of the 20 serum antibody-positive cases, RT-PCR-SH detected 18 positive cases, while ISH and IHC detected 19 and 16 positive cases, respectively. Of the 16 serum antibody-negative cases, RT-PCR-SH detected 8 positive cases while ISH and IHC detected 8 and 11 positive cases, respectively. A positive ISH signal for HCV was also detected in some lymphocytes and bile ducts in the liver. These results show that ISH with a highly specific riboprobe is comparable to RT-PCR-SH for detection of HCV infection in liver tissue.

Biopsy↗

PubMed2003

Beta1 subunits facilitate gating of BK channels by acting through the Ca2+, but not the Mg2+, activating mechanisms.

The beta1 subunit of BK (large conductance Ca2+ and voltage-activated K+) channels is essential for many key physiological processes, such as controlling the contraction of smooth muscle and the tuning of hair cells in the cochlea. Although it is known that the beta1 subunit greatly increases the open probability of BK channels, little is known about its mechanism of action. We now explore this mechanism by using channels in which the Ca2+- and Mg2+-dependent activating mechanisms have been disrupted by mutating three sites to remove the Ca2+ and Mg2+ sensitivity. We find that the presence of the beta1 subunit partially restores Ca2+ sensitivity to the triply mutated channels, but not the Mg2+ sensitivity. We also find that the beta1 subunit has no effect on the Mg2+ sensitivity of WT BK channels, in contrast to its pronounced effect of increasing the apparent Ca2+ sensitivity. These observations suggest that the beta1 subunit increases open probability by working through the Ca2+-dependent, rather than Mg2+-dependent, activating mechanisms, and that the action of the beta1 subunit is not directly on the Ca2+ binding sites, but on the allosteric machinery coupling the sites to the gate. The differential effects of the beta1 subunit on the Ca2+ and Mg2+ activation of the channel suggest that these processes act separately. Finally, we show that Mgi2+ inhibits, rather than activates, BK channels in the presence of the beta1 subunit for intermediate levels of Cai2+. This Mg2+ inhibition in the presence of the beta1 subunit provides an additional regulatory mechanism of BK channel activity.

Animals↗

PubMed2003

Differential expression of galectin-3 in pituitary tumors.

Galectin-3 (Gal-3), a beta-galactoside-binding protein, has been implicated in a variety of biological functions, including cell proliferation and differentiation, tumor cell adhesion, angiogenesis, apoptosis, tumor progression, and metastasis. We investigated the role of Gal-3 in the development and progression of pituitary tumors. Immunohistochemical and Western blot analysis of normal and neoplastic human pituitaries showed that only lactotroph (PRL) and corticotroph (ACTH) hormone-producing cells and tumors expressed Gal-3. Gal-3 was present in 24 of 38 (63.2%) PRL adenomas, 5 of 6 (83.3%) PRL carcinomas, 19 of 41 (46.3) ACTH adenomas, and 7 of 8 (87.5%) ACTH carcinomas, but not in 112 other pituitary adenomas and carcinomas. Pituitary folliculo-stellate cells, which have macrophage-type functions in the anterior pituitary, also expressed Gal-3. Hyperplastic and neoplastic pituitaries from p27(Kip1) (p27)-null mice, which produce mainly ACTH, showed increased Gal-3 expression levels compared with control mice. Treatment with transforming growth factor beta1, which regulates pituitary cell proliferation, reduced Gal-3 as well as p27 expression levels in cultured HP75 pituitary cells and Gal-3 in cultured pituitary cells from p27-null mice, suggesting that p27 is not necessary for the inhibitory effects of transforming growth factor beta1 on the cell cycle in the pituitary. The role of Gal-3 in pituitary cell function was examined by RNA interference experiments. Inhibition of Gal-3 gene expression by RNA interference decreased HP75 cell proliferation and increased apoptosis. These results indicate that Gal-3 has an important role in pituitary cell proliferation and tumor progression.

Adenoma↗