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M2M > Tissue Biology > Flashcards

Tissue Biology Flashcards

1
Q

What are the functions of mitochondria?

A
  1. generation of ATP
  2. apoptosis
  3. regulation of intracellular Ca2+ ions
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2
Q

What happens during fission & fusion in mitochondria?

A

Fusion plays a key role in repairing damaged mitochondria. Fission is required for mitophagy. Fusion and fission are both dependent on cellular GTPases: Mfn and OPA1 (fusion), as well as Fis1 and Drp (fission).

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3
Q

What are TOM and TIM in mitochondrial import?

A 
TOM = translocase of outer membrane 
TIM = translocase of inner membrane

Transport through TOM is passive, while transport through TIM is ATP-dependent

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4
Q

What does mtHsp70 do for mitochondrial import/export?

A

It helps get the protein through the pores in the inner membrane. The sequence is denatured as it comes through the pore, gets recognized by mtHsp70, binds to sequence & TIM, hydrolyzes ATP, pulls protein through membrane.

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5
Q

Describe the structure of ATP synthase in the mitochondrial membrane

A

2 main parts: F1 and F0.

F0 = inner mitochondria membrane; forms a proton channel
F1 = enzyme that makes ATP

Three protons are needed to generate one ATP molecule. Once made, ATP is transported out of mitochondria via the ATP-ADP antiporter

F1 contains 3 α and 3 β subunits. Spins around like a little motor –> goes through 3 conformations
1st conformation: binds ADP
2nd conformation: takes proton & ADP & squishes them together
3rd conformation: ATP gets released

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6
Q

What are the mechanisms of cell death regulated by mitochondria?

A

Cell damage induces Bak/Bax-dependent permeabilization of outer mitochondria membrane, leading to Cytochrome C release.

Cytochrome C then binds to several cytoplasmic proteins (if it’s oxidated!), forming a protein complex known as apoptosome. Apoptosome activates caspases, thus initiating apoptosis (regulated cell death). REVERSIBLE (via oxidation)

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7
Q

How do mitochondria promote necrotic cell injury?

A

Ischemic injury results in MPTP-dependent permeabilization of inner and outer mitochondria membranes, resulting in cytochrome release and elimination of proton gradient. Lack of protein gradient blocks ATP production. Furthermore, in the absence of a proton gradient, ATP synthase is converted into ATPase, thus using up available ATP. That leads to ATP depletion and necrosis. IRREVERSIBLE

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8
Q

How is mitochondria QC ensured?

A

First, several mitochondrial proteases, such as mAAA, iAAA and Lon are responsible for recognizing and degrading misfolded proteins.

Second, damage mitochondria can be “fixed” by fusing with healthy mitochondria, or can be fragmented & eliminated by mitophagy.

Finally, if mitochondria damage is extensive, mitochondria induce apoptotic cell death.

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9
Q

What are some of the mitochondria-related diseases?

A

Mutations in mitochondria fusion machinery causes autosomal dominant optic atrophy (OPA1 gene) and Charcot-Marie-Tooth neuropathy type 2A (Mfn2 gene).

Mutation in mAAA protease causes hereditary spastic paraplegia.

Finally, very potent toxin arsenic works by inhibiting oxidative phosphorylation and inhibiting ATP production.

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10
Q

What are the two layers of mucosae?

A

(1) the outer epithelium and (2) the CT directly underneath

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11
Q

What is the lamina propria?

A

The CT tissue directly under the epithelial lining of mucosa; contain many immune cells and small blood vessels

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12
Q

What is transcytosis?

A

The endocytosis of substances from one membrane region, followed by trans-cellular transport of the vesicles and their exocytosis from another membrane region

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13
Q

What are tight junctions and what do they do?

A

= the zonula occludens

Provide a highly selective barrier that limits or prevents diffusion of substances between epithelial cells.
Key proteins = occludins and claudins

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14
Q

What are adherens junctions?

A

= zonula adherens

Promote attachment, but also polarity, morphological organization and stem cell behavior within the epithelial sheet.

Proteins = specific cadherins that link to ACTIN filaments and other adapter/signaling proteins in the cytoplasm

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15
Q

What are desmosomes?

A

= macula adherens

Promote mechanical strength and resist shearing forces  and promote the structural organization of the epithelial sheet.
Proteins = a different class of cadherins that link to INTERMEDIATE filaments and other adapter proteins
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16
Q

What are microvilli?

A

Cell surface extensions (protrusions) that contain actin bundles connected to cytoskeletal elements in the cell interior. The primary function of microvilli is to increase surface area, which greatly increases the rate/efficiency of membrane transport and secretion.

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17
Q

What are stereocilia?

A

An unusual type of microvillus, found in the epididymus and sensory cells in the ear.
These are extremely long, actin-filled microvilli, and are NOT related to cilia.

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18
Q

What are cilia?

A

Microtubule-containing extensions

3 different kinds:
(1) A primary cilium is a single (one/cell) non-motile microtubule-based extension found on many different epithelial cell types. They help in signal transduction systems

(2) Motile cilia - wave like a boat oar to move mucous and other materials along passageways. Found in respiratory tract and oviduct
(3) Sensory cilia – are not motile and appear to function in sensory reception (e.g. in vestibular hair cells of the ear)

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19
Q

What are the components of the basal lamina?

A
  • collagen

- glycoproteins (laminins, entactin)

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20
Q

How are epithelial cells connected to the basal lamina?

A

Hemidesmosomes and focal adhesions on the basal surface of the epithelial cell to components of the basal lamina

Key class of proteins = integrins (distinct proteins from the cadherins that mediate cell-cell linkage). Specific integrins of hemidesmosomes connect to intermediate filaments in the epithelial cell. Different integrins of focal adhesions connect to actin filaments inside the epithelial cell.

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21
Q

What is the difference between endocrine and exocrine cells?

A
  1. Exocrine glands secrete materials onto epithelia-lined surfaces or the outside world.
  2. Endocrine glands secrete substances into the blood stream.
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22
Q

What are two ways that gland secrete their contents?

A

(1) Exocytosis (merocrine or apocrine glands)

2) Total cell disintegration (holocrine glands

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23
Q

What are the two components of all multicellular exocrine glands?

A

(1) Secretory units
- can be organized into bowl or flask-shaped lobules called alveoli or acini –> called alveolar or acinar glands
- organized into tubes –> called tubular glands

(2) Ducts - tubular structures that emanate from the secretory units

Secrete from APICAL membrane

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24
Q

What membrane do endocrine glands secrete from?

A

Hormone molecules must cross the basal surface and basal lamina of the epithelium (and finally the basal lamina and endothelial layer of the capillary) to reach the blood stream

= BASOLATERAL

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25
Q

What is the epithelial-to-mesenchymal transition?

A

Embryonic epithelia often disassemble and move into the mesenchymal (connective) tissues; there they may migrate to other locations to form new epithelia, or they may transform into distinct non-epithelial cell lineages that give rise to other tissues

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26
Q

What are transit amplifying cells?

A

Many stem cells produce daughters that also proliferate themselves, often at faster rates = transit amplifying cells
These transit amplifying cells then produce differentiated cells, either directly or through several steps of specification

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27
Q

What are some of the proteins that control development of many tissues during embryogenesis, fetal development, and childhood?

A

Wnt, Sonic Hedgehog, TGFβ, Notch, receptor tyrosine kinase family (RTK; for example the EGF receptors), and FGF receptor pathways

28
Q

What does Tarceva do?

A

It inactivates the EGF receptor and is commonly used to treat lung and pancreatic cancers

29
Q

What are carcinomas and adenocarcinomas?

A

Carcinoma = cancer of epithelial origin

Adenocarcinoma = cancer derived from glandular epithelium

30
Q

What are the genetics and underlying protein defects in cystic fibrosis?

A

Genetics: mutation in CFTR gene, which encodes the cystic fibrosis transmembrane conductance regulator protein

Autosomal recessive.
CF is a large gene on Chr 7. Over 1000 mutations have been identified; ΔF508 is the most common mutation

CFTR functions as a Cl- ion channel and controls the movement of salt and water into and out of cells

31
Q

What is the pathophysiology of CF?

A

The protein doesn’t move salt well, so you get dehydration of normal liquid that lines the lung

Impaired mucociliary clearance –> infection & inflammation –> bronchiectasis & lung damage –> functional lung impairment

32
Q

How do you diagnose CF?

A
  • Positive newborn screening OR
  • ≥1 clinical feature of CF OR
  • Family hx of CF
    PLUS
  • Sweat Cl ≥ 60 mmol/L AND/OR
  • 2 CF mutations
33
Q

What are the treatments for CF?

A
  • pancreatic enzymes to help them absorb food
  • daily techniques to clear out mucus (coughing techniques, inhaled medicines/antibiotics)
  • targeting common CF related bacteria
  • Daily salt supplement due to salt losses in sweat

Ivacaftor is a potentiator that works on the CFTR when it embeds in membrane but fails to open (G551D protein mutation)

Lumacafter is a corrector – prevents the cell from degrading improper protein, gets it to the membrane surface, and then Ivacafter helps open it up

34
Q

Where do many of the disease mutations occur in cilia?

A

The linkage domain – transition zone; acts as a gatekeeper of cilia

35
Q

What is the base anchor of cilia?

A

Basal body/centrioles – triplet microtubule structure

36
Q

What are the structural differences between motile cilia and primary cilia?

A

Primary cilia:

  • non-motile – instead, sensory
  • 9+0 axoneme

Motile cilia:

  • 9+2 axoneme –> 9 doublets on the outside
  • outer dynein arm –> generate mechanical force of ciliary beat pattern
  • radial spokes are involved in coordinating ciliary beat architecture itself
  • central pair of MT
37
Q

How are cilia assembled?

A

Centrioles are duplicated at the same time as DNA

The mother centriole becomes the basal body

Most of assembly of cilium is occurring in the cytoplasm of the cell, near the nucleus

Mother centriole –> has a series of distal appendages that recruit a vesicle from the Golgi = initiating event of new ciliogenesis –> doublet appendages form –> elongate. The structure needs to hit the plasma membrane & gets positioned –> axoneme forms

38
Q

What does the ciliary node do during development?

A

The ciliary node is an invagination of ciliated cells that forms during gastrulation on the midplate after anterior-posterior positioning is already established.

Nodal cilia possess a 9+0 organization, yet they beat in a rotary fashion to produce a net leftward flow of signaling molecules. The signals are then detected by non-motile sensory cilia that reside near the periphery of the ciliary node to signal organogenesis. This signaling is localized specifically to the future left axis of the body.

39
Q

What are the core “resident” cells in CT?

A

(i) Mesenchymal cells (mostly embryonic precursors) –> small numbers of them may persist through adulthood as stem cells
(ii) Fibroblasts
(iii) Myofibroblasts –> capable of smooth muscle-like function, and are found in connective tissues that require a contractile function.
(iv) Adipocytes
(v) Osteoblasts and osteocytes –> make bone
(vi) Chondrocytes –> make cartilage
(vii) Some smooth muscle cells

40
Q

What are the immigrant cells in CT?

A

WBCs that are produced from hematopoietic cells in the bone marrow:

a. Lymphocytes (acquired immunity)
b. Macrophages
c. Neutrophils and eosinophils (important for defense against microorganisms)
d. Mast cells (secretory cells –> important in edema and allergic hypersensitivities)
e. Osteoclasts (phagocytic cells; function in bone resorption and remodeling)

41
Q

What are the functions of macrophages?

A

(i) engulf (phagocytose) invading microorganisms
(ii) promote blood vessel formation (angiogenesis)
(iii) remodel damaged tissue
(iv) remodel normal developing tissue and organs as part of their morphogenesis

42
Q

What are the most abundant structural fibers of the ECM?

A

Collagen

43
Q

What are the 3 different types of collagen?

A

A. Fibrillar collagen

  • rope-like structures
  • have great strength to resist tensile stresses in tissues
  • most abundant in the body

B. Fibril-associated collagen

  • link collagen fibrils to each other
  • link fibrils to other tissue components

C. Network-forming collagen

  • very thin fibers (perhaps a few molecules thick)
  • assemble into interlaced networks that form porous sheets
  • found in the basal laminae, and also as anchoring fibers that attach basal lamina and cells to the ECM
  • some function as important filtration barriers (as in the kidney)
44
Q

What are the intracellular and extracellular modifications of collagen?

A

Intracellularly:

  • Collagen polypeptides are synthesized on the ER and translocated during synthesis to the ER lumen
  • Collagens are post-translationally modified (they are glycosylated and hydroxylated on selected amino acid residues)
  • The individual polypeptides are assembled into a triple helix

Extracellularly:

  • The N- and C-termini of collagen are cleaved by specific proteases. The N-terminal fragments that are generated are called N-telo peptides. The N-telo peptides are clinically important because their levels in urine and blood are used to diagnose important connective tissue and bone disease. Proteolytic release of these fragments is important to initiate:
  • Formation of bundles and end-to-end polymers of the collagen fibrils
  • Enzymes catalyze chemical cross-links between collagen molecules. These covalent cross-links can increase the tensile strength of the bundles
45
Q

What is the ground substance of the ECM composed of?

A

(1) Proteoglycans
(2) Other secreted proteins and glycoproteins = proteases that process collagen, other enzymes, growth factors, other polypeptide ligands
(3) Inorganic and small organic solutes (ions, carbohydrates, lipid, etc.)
(4) Water

46
Q

What is the structure of proteoglycans?

A

Proteoglycans contain a protein core attached to very large polysaccharides, called glycosaminoglycans (GAGs).

There are several different GAGs; most are covalently attached to proteins, but some like hyaluronic acid are not attached to a protein core. Proteoglycans are different from other glycoproteins because the GAG chains can be up to 95% of their mass.

47
Q

What are 3 important properties of GAGs?

A

(1) They are highly negatively charged. Consequently they are very hydrophilic (they attract lots of water)
(2) Their rigid extended structure causes them to readily form gels, which allow diffusion of small metabolites but inhibit large structures (like bacteria) –> act as sieves

Hydration creates a high swelling (turgor) pressure that allows the ECM to resist large compression forces (in contrast to collagen which functions to resist stretching forces).

(3) Some proteoglycans can also bind to and inactivate or activate other proteins, particularly growth factors and ECM modifying enzymes.

48
Q

What events occur in wounding & inflammation?

A

(1) Inflammation and blood clotting:
- platelets –> blood clots
- increased water –> swelling
- migration of monocytes, etc. into CT
- WBCs to wound
- proliferation of fibroblasts; differentiation of monocytes into macrophages

(2) New tissue formation
- fibroblasts divide and secrete ECM components
- division and differentiation of epithelial stem cells
- new blood vessel growth (angiogenesis), repair, and remodeling

(3) Tissue remodeling: Typically, the cellularity (density of cells) is reduced, and ECM becomes thinner and altered in organization.

49
Q

What is histamine secreted by, and why is it important?

A

Histamine secreted by MAST CELLS –> promotes endothelial permeabilization

50
Q

What is scar tissue?

A

Essentially disorganized epithelial/CT tissues lacking differentiated structural features of original tissue

51
Q

What cells make cartilage?

A

Chondrocytes

52
Q

What is the perichondrium?

A

An external layer of connective tissue that surrounds the cartilage

53
Q

What are the 3 types of cartilage?

A
  1. Hyaline cartilage
    - thin collagen fibrils + proteoglycans
    - irregular 3D pattern
    a. Allows metabolites to readily diffuse through the tissue.
    b. Promotes resiliency to compression forces during joint movement.
    c. Allows growth of chondrocytes and matrix from within the matrix.
    d. During growth, it can calcify and attract cells that initiate bone formation.
  2. Elastic cartilage
    - also thin collagen fibrils + proteoglycans
    - but also lots of elastic fibers & lamellae of elastic material
    - found in the external ear, in the epiglottis, and the larynx
    - does not calcify
  3. Fibrocartilage
    - large bundles of regularly arranged collagen –> similar to dense regular connective tissue
    - found where tendons attach to bones, and also in the intervertebral discs
    - designed to resist compression and sheer forces
54
Q

What are osteoprogenitor cells?

A

Stem cells –> generate osteoblasts and osteocytes

55
Q

What are osteoblasts?

A

CREATE BONE –> secrete osteoid

  • can divide
  • pinch off matrix vesicles, which contain enzymes that start calcification
56
Q

What are osteocytes?

A

HANG OUT IN BONE

  • derived from osteoblasts
  • encased by bone matrix in a lacuna
  • arrested in Go
  • extended processes called canaliculi –> send messages
57
Q

What are osteoclasts?

A

BONE EATERS

  • derived from monocytes – hematopoiesis
  • similar to macrophages

Several important functions:

  • degrade bone & matrix cartilage to allow growth of blood vessels ; promote remodeling
  • mobilize Ca2+ into the bloodstream

(3) They resorb bone for the purpose of mobilizing Ca2+ into the bloodstream (critical for maintaining proper Ca2+ concentrations in blood).

58
Q

How is bone matrix unique?

A

It contains hydroxyapatite = large amounts of a crystallized form of Ca2+ and PO4

59
Q

What are Haversian canals?

A

Channels that traverse the long axis through compact bone in long bones

Bone lamellae tend to surround a Haversian canal in concentric rings (like the rings of a tree); these lamellae and their canal are frequently referred to as a unit called the osteon

60
Q

What are Volkmann’s canals?

A

They link Haversian canals to each other and to the periosteum at the bone surface

61
Q

What are the two ways that bone is formed?

A
  1. Intramembranous ossification
    - no cartilage tissue present
    - groups of mesenchymal cells come together (condensation), transform into osteoprogenitors, which then differentiate into osteoblasts –> etc.
    - flat bones all form this way
  2. Endochondral ossification
    - using pre-made cartilage model
    - some cells in the perichondrium are converted to osteoprogenitors
62
Q

What is the difference between appositional and interstitial growth?

A

Appositional growth = at the surface

Interstitial Growth = growth from within

63
Q

How does cartilage get replaced by bone?

A
  1. On perichondrium of diaphyseal shaft of cartilage, collar of bone is formed
  2. Mesenchymal cells become osteoprogenitors, which become osteoblasts. Thus, perichondrium –> periosteum
  3. Cartilage matrix in that region becomes calcified
  4. Osteoclasts are recruited & degrade that calcified area
  5. Blood vessels grow into the degraded regions
  6. Osteoclasts + blood vessels go deeper & form a center of ossification (primary)
  7. Later, 2 new ossifications centers are established within both epiphyseal ends (secondary)
  8. At birth, only epiphyseal plates remain
64
Q

What are Bone Morphogenetic Proteins (BMPs)?

A

= short-range signals in the local bone environment

BMPs are proteins secreted by cells –> bind surface receptors and trigger intracellular protein phosphorylation that alters gene expression, which in turn promotes specific patterns of differentiation

65
Q

How does bone cell regulation control the blood levels of calcium?

A

= under tight regulation by endocrine hormones and dietary intake of calcium

Parathyroid hormone stimulates calcium liberation (bone resorption)

Calcitonin stimulates calcium uptake into bone (decrease in blood calcium levels)

Vitamin D is important for systems that promote calcium uptake from the intestine

66
Q

What is the structure & layers of blood vessels?

A
  1. Tunica intima
    - inner layer
    - layer of endothelial cells
    - (in larger arteries) inner layer of elastic/collagenous tissues
  2. Tunica media
    - middle layer
    - elastic laminae, SMOOTH MUSCLE, or collagen
  3. Tunica adventitia
    - collagenous tissue
    - (in larger vessels) –> vasa vasorum, or vessels of vessels. Supply oxygen & nutrients to outer layer
67
Q

Hypertrophic cardiomyopathy

A
  • mostly AD, incomplete penetrance, genetic heterogeneity
  • mutations in various components of the sarcomere
  • clinical presentations: cardiac murmur, cardiac “pump” failure, arrhythmia, sports/family screening

M2M (4 decks)

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